[Hypoxic pulmonary vasoconstriction and angiotensin II blockade in calves (author's transl)]. / Vasocostrizione polmonare ipossica e blocco dell'angiotensina II nel vitello.

The pulmonary vascular response to breathing low oxygen containing gas mixture was examined before and during Angiotensin II blockade in five open-chested newborn calves. Angiotensin II blockade was achieved by continuous infusion of Sar1-Ile5-Leu8-Angiotensin II (Saralasin), a competitive inhibitor of Angiotensin II. The hypoxic rise in pulmonary vascular resistance after blockade did not differ from that of control. It is concluded that Angiotensin II does not play a significant role in acute hypoxic pulmonary vasoconstriction in the calf.

The effect of changes in dietary sodium on lung and serum antiotensin-I-converting enzyme in the rat.

Three groups of rats were fed a sodium-deficient diet, a normal sodium diet, and a diet high in sodium for up to 8 weeks. Animals on a sodium-deficient diet had a significant decrease of serum sodium levels with a concomitant increase of renal renin granules. The reverse was true in rats on a high sodium diet whereas no significant changes in renin granulation were seen in rats fed a normal sodium diet. The changes in serum sodium levels and in number of renal renin granules were not associated with changes in lung or serum angiotensin-I-converting enzyme activity which did not vary significantly in any of the three groups of rats throughout the experiment. It is, therefore, suggested that such activity is independent of changes in sodium balance sufficient to affect the renal renin content.

Plasma angiotensin II levels in hypoxic and hypovolemic stress in unanesthetized rabbits.

Plasma levels of angiotensin II were determined by radioimmunoassay in unanesthetized white rabbits exposed to acute hypoxia (FIO2 10% for 10 min), chronic hypoxia (0.5 atm up to 16 days), or hypovolemic stress (bleeding 20 ml/kg). Angiotensin II levels significantly decreased after 10 min of acute hypoxia in normal rabbits and significantly increased when the same procedure was applied to animals previously exposed to hypoxia by 6-8 days of permanence in the hypobaric chamber or sodium deprivation. Chronic hypoxia resulted in a temporary increase of angiotensin II already evident on the 3rd day, but maximal at the 9th day with return to normal values within 16 days. Hypovolemic stress resulted in the expected rise of angiotensin II levels 10 min postbleeding both in normal and acclimatized rabbits. The response of the renin-angiotensin-aldosterone system to hypoxic and hypovolemic stress is different. The direction and magnitude of the response to hypoxia depends on the underlying state of activation of the system and the cardiovascular condition of the animal at the time of hypoxic stress.

Echocardiographic diagnosis of double-outlet right ventricle.

An echocardiographic technique (V scan) for confirming the diagnosis of double-outlet right ventricle is described. The technique demonstrates a frequent pathologic feature of double-outlet right ventricle, ie, origin in both great arteries side by side and anterior to the ventricular septum. The V scan offers greater diagnostic accuracy than the mere demonstration of mitral-semilunar valvular discontinuity.

Angiotensin I-converting enzyme and angiotensin II levels in women receiving an oral contraceptive.

In 11 healthy, normotensive young women taking contraceptive medication (Enovid) for at least one year, plasma levels of angiotensin II were significantly higher than in healthy male and female controls. No significant difference was seen in the serum activity of angiotensin I-converting enzyme measured in vitro. Although serum angiotensin I converting enzyme activity is stimulated in several conditions in which other components of renin-angiotensin-aldosterone system are increased, this is not the case during administration of estrogens.

Angiotensin-I-converting enzyme activity in idiopathic respiratory distress syndrome of the newborn infant and in experimental alveolar hypoxia in mice.

Serum angiotensin-I-converting enzyme activity was found to be elevated in infants with idiopathic respiratory distress syndrome when compared with healthy premature infants, normal infants, and acutely ill full-term infants. Serum and lung CE activity has been found to be elevated in mice exposed to hypobaric alveolar hypoxia which also stimulated renal renin production. These findings suggest that alveolar hypoxia stimulates the renin-angiotensin-aldosterone system and this system may be involved in the response to the stress of IRDS.

Prevention of pulmonary vascular changes of chronic alveolar hypoxia by inhibition of angiotensin I-converting enzyme in the rat.

To test the hypothesis that the renin-angiotensin system is involved in the development of the pulmonary vascular patholigic changes of chronic alveolar hypoxia, two groups of rats were exposed to 0.5 atm. for 21 days. One group received SQ 20,881 (2 mg. per kg.) every 8 hours subcutaneously and the second group received normal saline. A third group of rats was maintained at normobaria. Rats receiving SQ 20,881 had significantly less pulmonary arterial hypertrophy and right ventricular hypertrophy than hypobaric animals. SQ 20,881-treated rats showed a significant increase in adrenal weight but a marked reduction in the thickness of the zona glomerulosa, as compared with the other groups. Our findings indicate that angiotensin II is necessary in the development of the pulmonary vascular structural changes of chronic alveolar hypoxia.