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101. Pathways for angiotensin-(1--7) metabolism in pulmonary and renal tissues

Author

ALLRED, ALICIA J., DIZ, DEBRA I., FERRARIO, CARLOS M., and CHAPPELL, MARK C.

Subjects
Angiotensin -- Physiological aspects, Angiotensin converting enzyme -- Physiological aspects, Aminopeptidases -- Physiological aspects, Lisinopril -- Physiological aspects, Biological sciences
Abstract

Allred, Alicia J., Debra I. Diz, Carlos M. Ferwario, and Mark C. Chappell. Pathways for angiotensin-(1--7) metabolism in pulmonary and renal tissues. Am J Physiol Renal Physiol 279: F841-F850, 2000.--Two of the primary sites of actions for angiotensin (ANG)-(1-7) are the vasculature and the kidney. Because little information exists concerning the metabolism of ANG-(1-7) in these tissues, we investigated the hydrolysis of the peptide in rat lung and renal brush-border membrane (BBM) preparations. Radiolabeled ANG-(1-7) was hydrolyzed primarily to ANG-(1-5) by pulmonary membranes. The ANG-converting enzyme (ACE) inhibitor lisinopril abolished the generation of ANG-(1-5), as well as that of smaller metabolites. Kinetic studies of the hydrolysis of ANG-(1-7) to ANG-(1-5) by somatic (pulmonary) and germinal (testes) forms of rat ACE yielded similar values, suggesting that the COOH-domain is responsible for the hydrolysis of ANG-(1-7). Pulmonary metabolism of ANG-(1-5) yielded ANG-(3-5) and was independent of ACE but may involve peptidyl or dipeptidyl aminopeptidases. In renal cortex BBM, ANG-(1-7) was rapidly hydrolyzed to mono- and dipeptide fragments and ANG-(1-4). Aminopeptidase (AP) inhibition attenuated the hydrolysis of ANG-(1-7) and increased ANG-(1-4) formation. Combined treatment with AP and neprilysin (Nep) inhibitors abolished ANG-(1-4) formation and preserved ANG-(1-7). ACE inhibition had no effect on the rate of hydrolysis or the metabolites formed in the BBM. In conclusion, ACE was the major enzymatic activity responsible for the metabolism of ANG-(1-7) in the lung, which is consistent with the ability of ACE inhibitors to increase the half-life of circulating ANG-(1-7) and raise endogenous levels of the peptide. An alternate pathway of metabolism was revealed in the renal cortex, where increased AP and Nep activities, relative to ACE activity, promote conversion of ANG-(1-7) to ANG-(1-4) and smaller fragments. angiotensin-converting enzyme; neprilysin; lisinopril; SCH-39370; aminopeptidase; amastatin

Published
2000

102. Differential actions of renal ischemic injury on the intrarenal angiotensin system

Author

ALLRED, ALICIA J., CHAPPELL, MARK C., FERRARIO, CARLOS M., and DIZ, DEBRA I.

Subjects
Physiology -- Research, Kidneys -- Research, Angiotensin -- Receptors, Ischemia -- Physiological aspects, Biological sciences
Abstract

Allred, Alicia J., Mark C. Chappell, Carlos M. Ferrario, and Debra I. Diz. Differential actions of renal ischemic injury on the intrarenal angiotensin system. Am J Physiol Renal Physiol 279: F636-F645, 2000.--The present study determined the effect of either occlusion of the left renal artery for 60 min (ischemia) or sham operation on angiotensin (ANG) receptors and tissue and urinary levels of ANG peptides between 24 and 72 h recovery in male Sprague-Dawley rats. At 24 h postischemia, urinary concentrations of ANG I and ANG-(1-7) rose by an average of 83 and 64%, respectively (P [is less than] 0.05) but had declined to control levels by 72 h. Tissue ANG II rose at 24 h in postischemic kidneys by an average of 63% compared with the contralateral nonischemic kidney (P [is less than] 0.05). Whereas the enzymatic activity of angiotensin-converting enzyme and neprilysin was reduced after ischemia, renal renin activity in ischemic kidneys rose by 74% compared with sham-operated kidneys. Receptor autoradiography using [sup.125]I-labeled [[Sar.sup.1],[Thr.sup.8]ANG II ([sup.125]I-Sarthran) (0.8 nM) revealed a decreased apparent density of ANG receptors ([is greater than] 80% [AT.sub.1]) in ischemic kidneys with a trend for a decrease in the contralateral nonischemic kidneys compared with the kidneys from sham-operated rats. Twenty-four hours after ischemia, ANG II receptors decreased by 68% in glomeruli (P [is less than] 0.05), 49% in the outer cortical tubulointerstitial area (P [is less than] 0.05), and 48% in the inner cortical-outer medullary area of the vasa recta (P [is less than] 0.05). Medullary binding decreased ~50% in both the ischemic kidney and the contralateral nonischemic kidney compared with sham. In all regions of the ischemic kidney, receptors recovered by 72 h to levels not different from sham control rats. The marked change in urinary ANG I and ANG-(1-7) at 24 h following occlusion indicates these peptides may be potential urinary markers for acute renal ischemia. The reduction of receptors in vascular and tubular regions of the ischemic kidney provides a mechanism for the loss of vasoconstrictor responses to ANG II following ischemia previously reported by others. angiotensin II; angiotensin-(1-7), angiotensin receptors; [AT.sub.1] receptor; [AT.sub.2] receptor; renal ischemia; urinary angiotensins

Published
2000

111. The Brain Renin-Angiotensin System and Mitochondrial Function: Influence on Blood Pressure and Baroreflex in Transgenic Rat Strains

Author

Nautiyal, Manisha, Arnold, Amy C., Chappell, Mark C., and Diz, Debra I.

Subjects
Article Subject, cardiovascular system, hormones, hormone substitutes, and hormone antagonists
Abstract

Mitochondrial dysfunction is implicated in many cardiovascular diseases, including hypertension, and may be associated with an overactive renin-angiotensin system (RAS). Angiotensin (Ang) II, a potent vasoconstrictor hormone of the RAS, also impairs baroreflex and mitochondrial function. Most deleterious cardiovascular actions of Ang II are thought to be mediated by NADPH-oxidase- (NOX-) derived reactive oxygen species (ROS) that may also stimulate mitochondrial oxidant release and alter redox-sensitive signaling pathways in the brain. Within the RAS, the actions of Ang II are counterbalanced by Ang-(1–7), a vasodilatory peptide known to mitigate against increased oxidant stress. A balance between Ang II and Ang-(1–7) within the brain dorsal medulla contributes to maintenance of normal blood pressure and proper functioning of the arterial baroreceptor reflex for control of heart rate. We propose that Ang-(1–7) may negatively regulate the redox signaling pathways activated by Ang II to maintain normal blood pressure, baroreflex, and mitochondrial function through attenuating ROS (NOX-generated and/or mitochondrial).

Published
2013
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112. Angiotensin-(1-7) Blockade Attenuates Captopril- or Hydralazine-Induced Cardiovascular Protection in Spontaneously Hypertensive Rats-Treated with L-NAME

Author

Benter, Ibrahim F., Yousif, Mariam H. M., Al-Saleh, Fatemah M., Chappell, Raj Raghupathy Mark C., and Diz, Debra I.

Subjects
Blood Glucose, Leptin, Male, Captopril, Blood Pressure, Myocardial Reperfusion Injury, In Vitro Techniques, Kidney, Article, Ventricular Function, Left, Rats, Inbred SHR, Animals, Insulin, cardiovascular diseases, Antihypertensive Agents, Angiotensin II, Brain, Heart, Hydralazine, Myocardial Contraction, Peptide Fragments, Rats, Perfusion, Proteinuria, NG-Nitroarginine Methyl Ester, Hypertension, cardiovascular system, Cytokines, Angiotensin I, circulatory and respiratory physiology
Abstract

We assessed the contribution of angiotensin-(1-7) [Ang-(1-7)] to captopril-induced cardiovascular protection in spontaneously hypertensive rats (SHRs) chronically treated with the nitric oxide synthesis inhibitor NG-nitro-L-arginine methyl ester (SHR-l). NG-nitro-L-arginine methyl ester (80 mg/L) administration for 3 weeks increased mean arterial pressure (MAP) from 196 ± 6 to 229 ± 3 mm Hg (P0.05). Treatment of SHR-l with Ang-(1-7) antagonist [d-Ala7]-Ang-(1-7) (A779; 744 μg·kg(-1)·d(-1) ip) further elevated MAP to 253 ± 6 mm Hg (P0.05 vs SHR-l or SHR). Moreover, A779 treatment attenuated the reduction in MAP and proteinuria by either captopril (300 mg/L in drinking water) or hydralazine (1.5 mg·kg(-1)·d(-1) ip). In isolated perfused hearts, the recovery of left ventricular function from global ischemia was enhanced by captopril or hydralazine treatment and was exacerbated with A779. The Ang-(1-7) antagonist attenuated the beneficial effects of captopril and hydralazine on cardiac function. Recovery from global ischemia was also improved in isolated SHR-l hearts acutely perfused with captopril during both the perfusion and reperfusion periods. The acute administration of A779 reduced the beneficial actions of captopril to improve recovery after ischemia. We conclude that during periods of reduced nitric oxide availability, endogenous Ang-(1-7) plays a protective role in effectively buffering the increase in blood pressure and renal injury and the recovery from cardiac ischemia. Moreover, Ang-(1-7) contributes to the blood pressure lowering and tissue protective actions of captopril and hydralazine in a model of severe hypertension and end-organ damage.

Published
2011

113. Angiotensin Signaling in Cardio-Renal Disease: Angiotensin Peptides and Central Autonomic Regulation

Author

Diz, Debra I., Arnold, Amy C., Nautiyal, Manisha, Isa, Katsunori, Shaltout, Hossam A., and Tallant, E. Ann

Subjects
Aging, Medulla Oblongata, MAP Kinase Signaling System, Angiotensin II, Brain, Blood Pressure, Baroreflex, Autonomic Nervous System, Article, Peptide Fragments, Phosphatidylinositol 3-Kinases, Hypertension, Animals, Humans, Angiotensin I
Abstract

Aging, hypertension, and fetal-programmed cardiovascular disease are associated with a functional deficiency of angiotensin (Ang)-(1-7) in the brain dorsomedial medulla. The resulting unrestrained activity of Ang II in brainstem regions negatively impacts resting mean arterial pressure, sympathovagal balance, and baroreflex sensitivity for control of heart rate. The differential effects of Ang II and Ang-(1-7) may be related to the cellular sources of these peptides as well as different precursor pathways. Long-term alterations of the brain renin-angiotensin system may influence signaling pathways including phosphoinositol-3-kinase and mitogen-activated protein kinase and their downstream mediators, and as a consequence may influence metabolic function. Differential regulation of signaling pathways in aging and hypertension by Ang II versus Ang-(1-7) may contribute to the autonomic dysfunction accompanying these states.

Published
2011

121. Mechanisms of Human Erythrocytic Bioactivation of Nitrite

Author

Liu, Chen, primary, Wajih, Nadeem, additional, Liu, Xiaohua, additional, Basu, Swati, additional, Janes, John, additional, Marvel, Madison, additional, Keggi, Christian, additional, Helms, Christine C., additional, Lee, Amber N., additional, Belanger, Andrea M., additional, Diz, Debra I., additional, Laurienti, Paul J., additional, Caudell, David L., additional, Wang, Jun, additional, Gladwin, Mark T., additional, and Kim-Shapiro, Daniel B., additional

Published
2015
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127. Abstract 462: Effect of Adding Beet Root Juice to Exercise on Physical Performance and Cardiovascular Measures in Old Hypertensive Subjects

Author

Shaltout, Hossam A, primary, Marsh, Anthony P, additional, Laurienti, Paul, additional, Basu, Swati, additional, Klebous, Cassandra C, additional, Kus, Nicole, additional, Morgan, Ashley, additional, DosSantos, Patricia C, additional, Norris, James L, additional, Miller, Gary, additional, Rejeski, Jack, additional, Hawfield, Amret T, additional, Diz, Debra I, additional, and Kim-Shapiro, Daniel B, additional

Published
2014
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144. Effects of Resistance Training With and Without Caloric Restriction on Arterial Stiffness in Overweight and Obese Older Adults.

Author

Jefferson, Margie E., Nicklas, Barbara J., Chmelo, Elizabeth A., Crotts, Charlotte I., Shaltout, Hossam A., Diz, Debra I., Marsh, Anthony P., and Brinkley, Tina E.

Subjects
ARTERIAL diseases, LOW-calorie diet, RESISTANCE training, OVERWEIGHT persons, WEIGHT loss, ELASTICITY (Physiology), SYSTOLIC blood pressure, HEALTH
Abstract

BACKGROUND Arterial stiffness is an important marker of vascular aging that is increased in sedentary, obese older adults. Weight loss induced by caloric restriction (CR) can improve arterial stiffness in this population; however, the effects of resistance training (RT) are not clear. This pilot study determined the effects of RT with and without CR on arterial stiffness in overweight and obese older adults. METHODS Participants (mean age = 68 ± 3 years, mean body mass index = 31.1 ± 2.7 kg/ m2, 56% female, 13% Black) were randomly assigned to 3 days/week of supervised moderate-intensity RT (n = 16) or RT+CR (n = 16) for 5 months. Three indices of arterial stiffness were measured: brachial-ankle pulse wave velocity, large artery elasticity, and small artery elasticity. RESULTS Body mass was significantly reduced in the RT+CR group compared to the RT group (-6.2 ± 4.8 vs. 0.2 ± 1.2 kg, P = 0.0006). Within-group analyses showed that none of the arterial stiffness measures changed with RT or RT+CR. There were also no significant between-group differences, though median changes in large artery elasticity were slightly greater with RT+CR: 0.7 (-2.5, 5.1) vs. 0.3 (-2.6, 0.9) ml/mm Hg × 10, P = 0.07. Changes in large artery elasticity were negatively correlated with changes in waist circumference (r = -0.36, P < 0.05), systolic blood pressure (r = -0.38, P = 0.03), and diastolic blood pressure (r = -0.41, P = 0.02). CONCLUSIONS The combination of RT and CR, leading to a modest amount of weight loss (7%), tended to increase large artery elasticity more than RT alone. Our data suggest that reductions in waist circumference and blood pressure may promote improvements in elasticity. [ABSTRACT FROM AUTHOR]

Published
2016
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