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The inhabitancy in Far North increases a probability of development of coronary heart disease, acute myocardial infarction and arterial hypertension. Catecholamines and NO deficiency play a substantial role in the development of cold hypertension but are not involved in acclimatization cardiac hypertrophy. Data of in vivo experiments indicate in favor of an involvement of α-adrenergic receptors (ARs) in the mechanism of an appearance of cold hypertension. Cold acclimatization promotes an elevation of β3-AR density and decrease in β1-AR and β2-AR quantity on sarcolemma of cardiomyocytes. Experimental data indicate about the important role of aldosterone and angiotensin-II in the development of acclimatization hypertension. Catecholamines, aldosterone and angiotensin-II are not involved in cold hypertrophy of heart. Experimental data say on the important role of endothelin ETA-receptor in the formation of cold hypertrophy of heart and cardiofibrosis. Thyroid hormones play substantial role in the development of cold hypertension and cardiac hypertrophy.

The phylogenetic theory of general pathology postulates that in physiology and pathology the concepts of biological role of arterial tension had been subjected to inversion. The activation by nephron of synthesis of components rennin-angiotensin II and increasing of aldosterone secretion are directed not to increase arterial tension but to preserve volume of piece of third world ocean privatized by each entity as pool of intercellular medium where all cells continue to live as billions years before. In phylogenetic sense, early organs can't regulate effect of physical factor of regulation of metabolism the late one in phylogenesis of arterial tension. The cause of increasing of arterial tension is the vasomotor center but not the kidneys. The vasomotor center increases arterial tension in the proximal section and further hydrodynamic tension in the distal section of arterial stream and tends to resuscitate function of nephrons, biological function of endoecology and biological reaction of excretion. The arterial tension, besides the main role in biological function of locomotion, is a physical factor of compensation of disorders of biological functions of homeostasis, trophology, endoecology and adaptation. In phylogenesis, three levels of metabolism regulation has been developed The specific regulation of biochemical reactions occurs on autocrine level. In paracrin regulated cell cenosises, at distal section of arterial stream, metabolism is regulated by billions of local peristaltic pumps through compensation of biological reaction of endothelium-depended vasodilatation, micro-circulation, effect of humoral mediators and hormonal principles. In vivo, from the level of vasomotor center, metabolism non-specifically and systemic regulates physical factor-arterial tension through sympathetic activation of heart. The arterial tension in proximal section of arterial stream overcomes resistance and physically "forces through" arterioles with disordered micro-circulation. The angiotensin II is a vasoconstrictor only in distal section of arterial stream. In the process of pathogenesis of essential metabolic arterial hypertension the paracrin cenosises of nephron and kidneys are secondary involved into realization of pathological compensation and very often are "guilty without guilt" as such another "target organs" as brain, lungs and heart as well.

Possible involvement ofcalmodulin in adrenergic and serotoninergic regulation of vascular contractility has been studied. Calmodulin inhibitors trifluoperazine and W-13 suppress vasoconstriction of the rat aorta in response to norepinephrine, serotonin, and serotonin 5HT1A- and 5HT2A-receptor agonists (8-OH-DPAT and DOI, respectively) and do not affect the vasodilatory effect of 5HT1B-, 5HT2B-, and 5HT4-receptors. The force of aorta contraction in response to 8-OH-DPAT increases after the activation of calcium entry through voltage-gated Ca2+-channels. This effect is not related to non-specific activation of alpha1-adrenoceptors, since it is realized in the presence of prazosin. The inhibitor of calmodulin-dependent myosin light chain kinase KN93 decreases the vasoconstrictive response in response to norepinephrine and serotonin by only 20%. Calmodulin inhibitors slightly decrease aortic constriction in response to endothelin-1, vasopressin, angiotensin II, and KCl. Trifluoperazine does not suppress vasoconstriction induced by the G-protein activator AlF4(-). It is assumed that the target of trifluoperazine and W-13 is calmodulin interacting directly with alpha1-adrenoceptors and serotonin 5HT1A- and 5HT2A-receptors.

It has been shown that the agonist of 5HT1A-receptors 8-OH-DPAT induces contraction of aortic rings in the presence of angiotensin II. This effect is not associated with activation of alpha1-adrenoceptors by 8-OH-DPAT as it is reproduced in the presence of prazosin which completely suppresses the nonspecific vasoconstrictive effect of 8-OH-DPAT via alpha1-adrenoceptors on the aorta incubated without angiotensin II. Synergism in the action of angiotensin II and 8-OH-DPAT is completely preserved after partial desensitization of the receptors of angiotensin II. It has been found that 8-OH-DPAT increases the free cytoplasmic calcium concentration in cultured smooth muscle cells from the rat aorta. The data obtained support the hypothesis about the existence of "silent" vasoconstrictive 5HT1A-receptors. It has been suggested that activation of these receptors underlies synergism in vasoconstrictive action of serotonin and angiotensin II.

Influence of enalaprilat, angiotensin converting enzyme inhibitor, on a functional proteinuria associated with increase in diuresis unduced by furosemide, 1-deamino-arginine vasotocin (1d-AVT) injection or water loading was investigated in experiments with Wistar rats. Intraperitoneal injection of 0.1 mg/100 g b.w. of enalaprilat resulted in reduction of glomerular filtration rate, solute-free water reabsorption and solutes excretion, particularly potassium excretion, after 1d-AVT administration and decrease in diuresis and solute-free water excretion after oral water loading. Enalaprilat injection did not influence on the level of proteinuria induced by the various types ofdiuresis and albuminuria during water diuresis and 1d-AVT-dependent saluresis. The data obtained have shown that decrease in angiotensin II production in the renal structures does not affect protein excretion rate during examined forms of proteinuria and suggest existence of a multicomponent system of the pressure stabilization in the glomerular apparatus.

Apelin is an endogenic ligand of apelin (APJ) receptors widely expressed in human tissues. This protein is a peripheral vasodilator having a powerful positive inotropic action on myocardial contractility. This review describes mechanisms of interaction and apelin role in health and pathology.

We compared activity of synthetic complexes of angiotensin II and functionally different proteins (transport protein, serum albumin and neurospecific Ca2+-binding protein S100b) as analogues of endogenous protein-peptide complexes. Physiological activity of angiotensin II was specifically modified by these proteins. It was hypothesized that the complex of angiotensin II and S100b is primarily involved in the regulation of hemodynamics, whereas the complex of angiotensin II and bovine serum albumin plays a role in the formation and realization of drinking behavior.

Results from experimental studies suggested a significance of the nitric oxide (NO)-cGMP- and cAMP-pathways in the control of the function of the smooth musculature of the human prostate. In addition, it has also been assumed that the vasoconstrictory peptide endothelin-1(ET-1) may play a role in the dynamic component of benign prostatic hyperplasia (BPH) and the so-called lower urinary tract symptomatology (LUTS). Nevertheless, up till now, little is known as to potential interactions between the contraction of prostatic smooth muscle mediated by ET-1 and the relaxation induced by NO and cGMP. Thus, it was the aim of the study to elucidate the effects of drugs interfering with the cGMP-pathway on the tension induced by ET-1 of isolated human prostate tissue, as well as contractile responses of isolated strip preparations to ET-1 and angiotensin-II (AT-II). Macroscopically normal human prostate tissue from the transition zone was obtained from male patients who had undergone surgery for localized cancer of the prostate or urinary bladder. Using the organ bath technique, the ability of ET-1 and AT-II to contract isolated prostate strips was evaluated. In another set-up, the effects of the NO-donor S-nitrosogluthatione (GSNO) and C-type natriuretic peptide(CNP), known as an endogenous ligand of the membrane bound guanylyl cyclase, (1 nM-1/10 microM) on the tension induced by 0.1 microM ET-1 of human prostate strips were investigated. The adenylyl cyclase stimulating agents forskolin and NO-donor natrium nitroprusside (NNP) were used as reference compounds. While AT-II failed to contract the prostate tissue, ET-1 induced stable and reproducible contractions of the tissue strips. The tension induced by 0.1 microM ET-1 was dose-dependently reversed by the drugs. The rank order of efficacy was forskolin >NNP>CNP(1 microM)>GSNO. R(max) values ranged from 55% (forskolin) to 35% (GSNO). Forskolin was the only compound which reached an EC50 value. Our results demonstrate that drugs in terfering with the cGMP- and cAMP-pathways can reverse the tension induced by ET-1. These findings are in support of the hypothesis that both cGMP and cAMP contribute to the control of the prostate smooth muscle tension and may provide new strategies for the future pharmacotherapy of LUTS und BPH.

The intravenous injections of enalapril maleate (0.1 and 0.5 mg/kg) and losartan (0.5 and 2.5 mg/kg) produced a 22-32% decrease in the size of myocardial infarction in rats with coronary ligation. This was accompanied by inhibition of the lipid peroxidation as revealed by the MDA test and Fe2+ induced chemiluminescence. Both drugs also increased the oxygen affinity of hemoglobin in the P50 test in vitro. Enalapril did not significantly alter the MDA level and superoxide dismutase (SOD) activity in the whole human blood. In contrast, losartan reliably inhibited SOD activity.

Enteropeptidase (enterokinase, EC 3.4.21.9) hydrolyzes peptide bonds formed by carboxyl groups of Lys or Arg residue provided that less than four negatively charged amino acid residues are in positions P2-P5 of its substrate. We determined the kinetic parameters of three substrates of this type: human angiotensin II (AT) (DR decreases VYIHPF) and the Hb(2-8) (LTAEEK decreases A) and Hb(1-9) (MLTAEEK decreases AA) peptides of the cattle hemoglobin beta-chain. The Km values for all the substrates (approximately 10(-3) M) were one order of magnitude higher than those of the typical synthetic substrates of enteropeptidase or chimeric proteins with the -DDDDK- full-size linker (Km approximately 10(-4) M). The kcat values for AT and Hb(2-8) were also close and low (approximately 30 min-1). The general hydrolysis efficiency of such substrates is no more than 1% of the corresponding value for the typical peptide and protein substrates of the enteropeptidase. However, the elongation of Hb(2-8) peptide by one amino acid residue from its N- or C-terminus results in a dramatic increase in the catalytic efficiency of the hydrolysis: the kcat value for Hb(1-9) is 1510 min-1, which means that it is hydrolyzed only three times less effective than the chimeric protein with the full-size linker.

Aim: To specify variable 24-h arterial hypertension (AH) stage II profile and to assess significance of pharmacological block of the end of the renin-angiotensin-aldosteron system for correction of the determined disorders., Material and Methods: The study was made of 46 men (mean age 42.8 +/- 3.28 years) with stage II AH and 25 normotensive controls (mean age 39.2 +/- 3.10 years). Depending on the magnitude of mean 24-h AP variability (APV), hypertensive patients were divided into two groups. Variability of systolic and/or diastolic AP (SAPV and DAPV, respectively) was considered high in at least 15.2 and/or 12.3 mm Hg variability, respectively, and normal at less values., Results: AP 24-h profile in men with AH stage II and high APV compared to patients with normal APV is characterized by higher frequency of AP rise and less frequency of its night fall. In patients with high APV the drug eprosartan (teveten) is more effective in correction of hypertension and night fall of AP., Conclusion: Eprosartan has an adequate corrective activity in relation to absolute values of SAP and DAP in different hours. The highest hypotensive activity of the drug was seen in persons with initially high circadian AP variability within 24 hours.

Aim: To study the effect a combination of enalapril and losartan on life quality in patients with congestive heart failure (HF)., Material and Methods: One hundred and eighty six patients with NYHA functional classes II to IV HF were examined. The study inclusion criteria were as follows: a left ventricular (LV) end-diastolic volume of > 160 ml, a LV ejection fraction of < 35%, sinus rhythm, a cardiothoracic index of > 0.55, no history data on prior treatment with an angiotensin-converting enzyme inhibitor (ACEI) and/or an AT1-antagonist, a patient's written free-will consent to participate in the study. The exclusion criteria were as follows: pacemaker migration, an artificial pacemaker, high-degree block, atrial fibrillation, cerebral circulatory disorders. All the patients were divided into 4 groups and received basic therapy with cardicet, 60-120 mg/day, aspirin, 250 mg/day, furosemide, 80-440 mg/week, and digoxin, 0.25-0.5 mg/day. Group 1 comprised 60 patients who refused therapy with ACEI and/or AT1-antagonist despite that they had indications for their use and they had been convinced many times. In Group 2 (n = 82) enalapril, an ACEI, was added to the basic therapy. Its initial dose of 2.5 mg/day was given once and slowly incremented to the therapeutical one (10-20 mg/day). Group 3 patients (n = 56) on the basic therapy were additionally treated with the AT1-antagonist losartan in a daily dose of 25-50 mg. They were started on 12.5 mg a day. In group 4 the basic therapy was added by a combination of enalapril and losartan in the same doses. The follow-up was 48 weeks. The efficiency of the treatments was controlled by the personal questionnaires SF-36, Life with Heart Failure, by evaluating the magnitude of clinical HF manifestations and by estimating the total life quality inxed. The data were analyzed by assuming that all the patients received the treatments., Results: As compared with the conventional therapy and the use of each drug alone, a combination of the ACEI enalapril and the AT1-antagonist losartan promotes a more significant increase in the satisfaction of the patients with their vital activity, in the critical rate of their self-assessment of the "internal picture" of disease, and leads to a greater improvement of the quality of their life as a whole., Conclusion: The ICAE-AT1-antagonist combination exerts a positive impact on life quality in patients with heart failure.

Aim: To study clinicogenetic determinants of left ventricular hypertrophy (LVH) regress in 52-week antihypertensive therapy to achieve the target arterial pressure (AP) < 140/90 mm Hg., Material and Methods: I/D-polymorphism of angiotensin converting enzyme gene, T174M-polymorphism of angiotensinogen gene, A1166C-polymorphism of angiotensin II ATI-receptor gene (ATII), 4a/b-polymorphism of endothelial NO-synthetase gene (eNOS) were determined in 64 patients (24 males, 40 females, mean age 54 +/- 1.1 years) with arterial hypertension (AH) and LVH. Echocardiography, laboratory tests, clinical measurements of blood pressure (BP) and 24-h AP monitoring were made after 4 weeks of placebo and 52 weeks of treatment., Results: Baseline values of LV myocardium mass index (LVMMI) correlated significantly with mean 24 hour and night systolic arterial pressure; 24-h, day and night pulse pressure (PP). In patients with regress of LVH the degree of LVMMI reduction significantly correlated with lowering of day and night PP, baseline level of neutrophils, uric acid and creatinine 52 weeks after treatment. Groups made by polymorphism, did not significantly differ by initial LVMMI, frequency of achievement of target AP. In patients with genotypes ID/II and aa, the level of achieved diastolic arterial pressure was significantly lower than in other groups. Resistant LVH was seen in 42.2% patients. Frequency of AP normalization was higher in the group of patients with LVH regress (48.6% vs 25.9%; p < 0.05). Resistant LVH occurred more frequently in patients with genotype DD (64.0 vs 28.2% in patients with II/ID, p < 0.05) and in patients with genotype 4ab (62.9 vs 30.4% in patients with genotype aa and 21.4%--with genotype bb; p < 0.05 in both cases). In patients with resistant LVH frequency of DD genotype increased (59.3 vs 24.3% in patients with regress of LVH; p < 0.01), genotype AA (74.5 vs 48.6%; p < 0.01) and genotype ab (63.0 vs 27.0%, p < 0.01)., Conclusion: Regress of LVH in AH patients depends on dynamics and complex interactions of some hemodynamic, laboratory and genetic parameters.

Allele and genotype frequency distribution patterns of the polymorphic regions at the genes for human endothelial NO-synthase (NOS3) (the ecNOS4a/4b VNTR and the Glu298Asp substitution) and the angiotensin II type 1 receptor (AT1)(the A1166C substitution) were compared in 83 unrelated healthy individuals and 88 patients with ischemic heart disease (IHD). In the group of patients statistically significantly higher frequencies of the NOS3 allele 4a (45.5 versus 19.3%), as well as the 4a/4a (15.9 versus 2.4%) and 4a/4b (59.1 versus 33.7%) genotypes were observed. Frequencies of the allele 4b (54.5% versus 80.7%) and the 4b/4b homozygotes (25.0 versus 63.9%) were statistically significantly lower in the group of IHD patients than in healthy individuals. The IHD patients were statistically significantly different from the healthy subjects also in the distributions of the AT1 genotypes. In the former group, a significantly decreased frequency of the AA homozygotes (51.1 versus 65.1%) and an increased frequency of AC heterozygotes (40.9 versus 27.7%) were observed. Thus, in the Moscow population the ecNOS4a/4b VNTR of the NOS3 gene and the A1166C polymorphism of the AT1 gene are associated with the IHD development. Furthermore, the correlation with the IHD revealed was much stronger for the NOS3 VNTR locus.

The experiments on 85 non-inbred rat males modelling proximal nephron section impairment--sublimate nephropathy--showed the existence of two pathogenetic mechanisms of TIC development: elevated level in the renal cortex of vasoconstrictive, collagen synthesis stimulating hormone angiotensin 2; weak fibrinolytic activity in the renal papilla underlying fibrin deposit in this renal zone followed by fibrin transformation in collagen.

The surface activity of angiotensin-2 was studied using the method of dynamical capacitor and Wilgelmi. Angiotensin was shown to possess the surface activity, forming well regulated insoluble monolayers of liquid-gas interfaces with peptide adsorption of 3.7 x 10(-6) M/sm2 and area of 0.45 nm2 per one molecule. It is assumed that due to these properties angiotensin-2 under physiological conditions can interact with molecules of the lipid matrix of biological membranes.

The studies of lipid monolayers showed the interaction of an angiotensin-2 and lipid monolayers to be a two-stage process. In the first stage peptide molecules were adsorbed due to electrical interaction in the plane of polar heads of lipid molecules. In the second stage peptide molecules incorporated into the lipid matrix owing to hydrophobic interactions. These results suggest that the lipid matrix may perform the function of a catalyst of the peptide-receptor interaction by changing the spatial structure of angiotensin molecules at the transition of the latter from hydrophobic environment.

A study of neurohumoral and functional determinants of the advance of Ischemic heart disease in 39 patients with unstable stenocardia with positive results of loading tests (transesophageal electrocardiostimulation and veloergometry) allowed to reveal a significant reduction of the coronary reserve and regional dysfunction of the myocardium that interrelated with changes of the prostacyclin/thromboxane balance, increase of vasopressin with unchanged angiotensin II value and increased marker of the functional state of thrombocytes--beta-thromboglobulin. These changes may be one of the leading links in the pathogenesis of destabilization.

The histamine-releasing activity of some linear and cyclic analogues of bradykinin (BK) and kallidin (K) was studied on rat peritoneal mast cells and compared with that of angiotensin (AT) cycloanalogues assayed earlier. Peptide cyclization, irrespective of the main pharmacological effect of the linear precursors (hypotensive for BK and K, hypertensive for AT), considerably enhanced their histamine-releasing activity. The activity of the tested compounds was found to depend on their amphiphilicity and cycle size. Linear AT and BK and their cycloanalogues bind to different receptor structures on rat mast cells. These findings suggest that BK, K and AT cycloanalogues belong to the same group of nonimmunological mast cell activators whose specific mechanism of action is based on the common structural features resulting from cyclization.

The action of two earlier isolated highly purified spleen thiol proteinases on angiotensins I and II, bradykinin and kallidin was investigated. It was demonstrated that proteinase I which is apparently cathepsin L from bovine spleen brings about rapid inactivation of angiotensin II with a splitting of the Tyr-Ile bond and a formation of two tetrapeptides. Proteinases I also split angiotensin I. Proteinase I partially inactivates bradykinin and kallidin by splitting the Gly4-Phe5 bond. The activity of proteinase I toward angiotensin II is about 50 times higher than that toward bradykinin. The corresponding values of Km and V are 7.5 X 10(-5) M and 10.0 mumole/min/mg. The possible role of proteinase I in angiotensin II inactivation under physiological conditions is discussed. Proteinase II converts kallidin to bradykinin by splitting off the N-terminal lysine. Proteinase II causes partial inactivation of bradykinin by splitting of the Gly4-Phe5 and Phe5-Ser6 bonds of this peptide. Proteinase II possesses both aminopeptidase and endopeptidase activities and is therefore cathepsin H from spleen. Proteinase II does not split either angiotensin I or angiotensin II.

Electron microscopic studies of the intersticial cells of the renal medullar layer and the count of lipid granules in them were conducted in two experimental states accompanied by a reduction of the circulating blood volume--72 hours of water-free diet and intravenous administration of Lazyx that possesses a potent natriuretic and diuretic effect. The concentration of renin and angiotensin was determined in the plasma of the same animals, using the radioimmunoassay technique, and the juxtaglomerular apparatus of the kidneys was examined. The study has demonstrated that the reduction of the circulating blood volume is accompanied, on the one hand, by a significant elevation of the plasma concentration of renin and angiotensin, and, on the other hand, by a reduction of the number of lipid granules in the intersticial cells that is interpreted by the authors as an index of an increased synthesis of renal prostaglandins. It has been concluded that a close functional interrelashionship exists between the two hormonal systems of the kidneys that regulate the water-electrolyte homeostasis, i.e. the renin-angiotensin system and the prostaglandins system.

The study concerns the effect of angiotensin II when infused into the systemic and portal blood flow upon the general and renal haemodynamics in normal dogs and in hypertensive animals, as well as the effect of the operation of porto-caval transposition upon the course of renovascular hypertension. When peptide is infused, at a rate that causes a moderate pressor effect, into the systemic blood flow of normal animals, an antidiuretic and antinatriuretic effect is obtained, in hypertensive animals--an increase of diuresis, natriuresis and a less distinct pressor effect are obtained. When angiotensin II is infused into the portal flow, a less distinct pressor and renal effect is seen in animals with renovascular hypertension. The operation of porto-caval transposition of the vessels results in a hypotensive effect in the animals with renovascular hypertension.

Carboxycathepsin from bovine kidney split the dipeptide fragments from the C-terminal part of peptides of different structure. Peptides containing the proline residue at the second position from the C-terminal amino acid residue and also peptides with substituted terminal alpha-carboxyl group were not hydrolyzed by carboxycathepsin. The enzyme was activated by Cl, Zn2+, Co2+ and Mn2+. The substances which formed the chelate complexes with ions of two-valent metals and also heavy metal ions, inhibited the enzymatic activity. Diisopropyl fluorophosphate did not inhibit carboxycathepsin. The homogeneous preparation of carboxycathepsin converted angiotensin 1 into angiotensin 11 and hydrolyzed bradikinine, splitting off C-terminal dipeptides consequentially.

The activity of blood plasma renin and the content of aldosterone were studied in dynamics in 55 patients with acute myocardial infarction following a different course. The dependence of renin activity and potassium content is analysed. The authors did not find any dependence between the degree of growth of blood plasma renin activity and the course of the disease; exception to this were patients with disorders of rhythm and conductivity. It is presumed that changes in potassium metabolism play an important role in the changes in renin activity in myocardial infarction.

Aggressive behaviour (muricidal) induced in rats by local electrolyte lesions of septal brain area was accompanied by changes in angiotensin-converting enzyme (ACE) and total kinin-destroying activity (KDA) in different brain regions. In 2-month-old rats (30 days after septal operation) a decrease in ACE activity was observed in hypothalamus and striatum, while in the cerebellum the activity was increased. KDA in this group of aggressive rats was markedly increased in the pituitary body, hypothalamus and striatum. Half a year after septal lesion in spite of aggressive behaviour retention, ACE activity and KDA did not differ from their activity in nonmuricidal rats of the same age. These data show a distinct role of the peptides studied in the formation and maintenance of muricidal behaviour in rats of different age.

Properties of the carboxycathepsin inhibitors teprotide, captopryl, enalacryl are considered. Presence of low molecular thermo- and acid stable carboxycathepsin inhibitors of peptide nature in blood serum and lymphocytes is discussed.

The examination of enzymes involved in the neuropeptides metabolism shows that the same substance can be hydrolysed by different peptidases. At the same time each of these enzymes can take part in destruction of different in their structure and functional significance peptides. The analysis of the conditions ensuring selective, regulating action of the definite neuropeptidases in the process of peptides formation and destruction is necessary for the understanding of the regulatory peptides physiological role. Substrate specificity of the enzyme, its localisation in some tissues and organs in brain and periphery, the organisation of enzyme or enzymatic complexes in a cell, the specific inhibitors influence are considered as such conditions. These conditions are examined for a number of peptidases involved in enkephalin metabolism, angiotensin I and II, bradykinin, substance P and others. The significance of such enzymologic approach in the investigation of regulatory peptides function is illustrated by concrete examples.

The activity of the renin-angiotensin system was studied in experiments on rats under conditions of the inhibited prostaglandin synthesis. It was found that the injection of indometacin in non-hypertensive doses was accompanied by a substantial lowering of the plasma renin activity and of the secretory function of the juxtaglomerular apparatus of the kidneys. The amount of lipid granules increased in the interstitial cells simultaneously, this reflecting the inhibition of prostaglandin synthesis in the medulla of the kidneys. The results of these experiments permit the assumption to be made that the renin synthesis in the juxtaglomerular apparatus was connected with the synthesis of renal prostaglanins.

The binding of angiotensin II and its analogues (13) to rabbit antibodies and glomerular cell receptors from rat adrenal cortex was studied, using the radioimmunoassay method and radioreceptor analysis. Double modifications introduced into the angiotensin structure were found to increase in an additive fashion its binding to the antibodies and renal cell receptors. The relative binding activity of the analogues carrying a double modification can be assessed if the activities of the analogues with the appropriate single modifications are known. It was concluded that the testing of modifications in the peptide structure for their additivity may provide some insight into the conformational properties of peptides during their binding to the protein.

Spontaneously muricidal rats (SMR) were selected from a group of white male rats. In the remaining animals muricide was induced by the local electrolyte damage of the brain septal area. Both muricidal models had different physiological indexes of aggressive reactions. In SMR a significant decrease in angiotensin-converting enzyme activity was detected in the midbrain and thalamus-hypothalamus areas. In the group of operated muricidal ("septal") rats alterations in angiotensin-converting enzyme activity have been revealed in none of the brain areas examined. The increase in total kinin-destroying activity in the pituitary, cerebellum, striatum and thalamus-hypothalamus areas was detected. The results indicate neurochemical specificity of brain angiotensin II and kinins in the regulation of different muricidal models.

It has been established that the catecholamine-induced increase in renin secretion by juxtaglomerular apparatus cells and sodium reabsorption stimulation in the rat kidney are consequent on the excitation of renal beta-adrenoreceptors. Strophanthin K interferes with the renin-secreting action of adrenaline and perverts its activating effect on sodium transport by renal tubules. When given in a dose inhibiting angiotensin II formation and renin-secreting effect of catecholamines, heparin also diminishes their activating effect on tubular sodium transport. It is suggested that the renin-angiotensin system may be directly involved into the mechanism of catecholamine-stimulated sodium reabsorption by the rat kidney.

In the hypokinetic study a certain correlation between variations in the means of the volume of cortical and juxtamedullary glomerules and the function of the juxtaglomerular apparatus has been established. It is hypothesized that at early hypokinesia renal vascular changes are nonspecific. The phenomenon of renal excretion of fluids and electrolytes is explained in terms of a simultaneous increase in the reninangiotensin activity and 11-hydroxycorticosteroid content in plasma.

The binding of the biologically active bradikinin analog--[125I]-tyr-B to partially purified fractions of plasma membranes from rat and rabbit aorta and from human umbilical veins and arteries has been studied. It was shown that some regions of vascular plasma membranes have a high affinity for the analog (Kac = 2--6.10(8) M-1). The capacity for competitive substitution of angiotensin II and [125I]-angiotensin II-tyr-B for [125I]-tyr-B suggests the similarity of the binding sites of plasma membranes of the two biologically active peptides--bradikinin and angiotensin II.