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Objective: To assess the effects of dihydralazine, labetalol and magnesium sulphate on the vascular tone in the isolated, perfused human placental cotyledon., Methods: In vitro perfusion of the fetal compartment of isolated, human placental cotyledons., Results: None of the drugs affected basal vascular tone. The thromboxane A2-mimic U46619 and endothelin-1 induced a concentration-dependent increment in perfusion pressure, while 5-hydroxytryptamine induced a variable increase, and norepinephrine induced a small, transient increase in perfusion pressure. After preconstriction with U46619, magnesium sulphate (1.5 x 10(-3) to 6 x 10(-3) mol/l) induced a decrease in perfusion pressure, while dihydralazine (10(-6) to 10(-4) mol/l) or labetalol (10(-7) to 10(-4) mol/l) enhanced the perfusion pressure. These effects of dihydralazine and labetalol were unaffected by treatment with indomethacin 10(-6) mol/l, but could be reversed by addition of magnesium sulphate 6 x 10(-3) mol/l. Labetalol 10(-6) to 10(-4) mol/l also caused an increase in the perfusion pressure induced by endothelin-1, but showed no effects after preconstriction with 5-hydroxytryptamine. Pretreatment with labetalol 10(-4) mol/l inhibited the transient increase in perfusion pressure induced by norepinephrine 3 x 10(-5) mol/l., Conclusions: The present data demonstrated that the commonly used vasodilating agents labetalol and dihydralazine do not produce vasodilatation in the human perfused cotyledon after vasoconstriction induced by agents of suggested importance for maintenance of fetal placental vascular tone, and that high concentrations of these drugs may even enhance vasoconstriction induced by thromboxane and endothelin-1 in this area. Magnesium sulphate may show the potential to reverse such unwanted effects of dihydralazine and labetalol.

In submaxillary sialoadenectomized and nephrectomized mice aggressive behaviour provoked 5 to 40-fold increases in plasma renin concentration. The changes in renin concentration with time were different in different groups of confronted mice with only partial correlation between the pattern and the observable degree of fight. The changes were similar in sialoadenectomized mice with untouched kidneys as in sialoadenectomized and nephrectomized, indicating that aggression causes no measurable, if any, renal renin release. Repeated aggression with 2 hourly intervals provoked repeated renin release from extrarenal and extrasubmaxillary sources. The renin concentrations of different organs showed the same mutual relationship as in other mammals, but were about 10-fold higher. Splenectomy was without effect on the aggression-provoked renin release. Antibodies against pure mouse renin neutralized the renin in plasma and organs, which contained only insignificant, if any, pepsin activatable inactive renin. Adrenaline, apomorphine, carbachol and dihydralazine were as isoprenaline and noradrenaline without effect on renin release in sialoadenectomized and nephrectomized mice.

The effect of acute hypertension and hypotension on serum TSH concentration was studied in anesthetized male rats. I.v. infusions (10 and 30 min) of Na-nitroprusside and dihydralazine induced a profound hypotension, and angiotensin amide and noradrenaline increased blood pressure, but none of the treatments significantly modified serum TSH concentrations. Also clonidine and noradrenaline, when given i.p., caused hypertension, but again the increase of serum TSH levels was not consistent. When the whole material was analysed, there was a scarcely significant correlation between the change of blood pressure and the change of serum TSH level. It is inferred that the drugs affecting TSH secretion, do not exert their action solely by changing the blood pressure.