Renal manifestations of NaCl sensitivity in borderline hypertensive rats

Compared with the normotensive Wistar-Kyoto rat, the spontaneously hypertensive rat exhibits exaggerated alterations in renal sympathetic nerve activity and excretory function during volume expansion (exaggerated natriuresis) and environmental stress (antinatriuresis). The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat and develops hypertension with increased dietary NaCl intake. The present investigation sought to determine whether the dietary NaCl intake-induced transition from the normotensive state of the Wistar-Kyoto parent to the hypertensive state of the spontaneously hypertensive parent in the borderline hypertensive rat was accompanied by a similar transition of the renal sympathetic nerve activity and excretory responses to volume expansion and environmental stress. Borderline hypertensive rats fed a 1% NaCl diet remained normotensive and exhibited renal sympathetic nerve activity and excretory responses to volume expansion and environmental stress that were similar to those of their Wistar-Kyoto parent. Borderline hypertensive rats fed an 8% NaCl diet developed hypertension and exhibited responses that were similar to those of their spontaneously hypertensive parent. Thus, the dietary NaCl intake-induced transition from the normotensive state of the Wistar-Kyoto parent to the hypertensive state of the spontaneously hypertensive parent in the borderline hypertensive rat was accompanied by a similar transition of the renal sympathetic nerve activity and excretory responses to volume expansion and environmental stress. The results suggest that increased dietary NaCl intake is able to induce or unmask the capabilities for these responses, which are genetically conveyed to the borderline hypertensive rat by the spontaneously hypertensive rat parent in latent forms.     

Localization of the action of cholera toxin on adenyl cyclase in mucosal epithelial cells of rabbit intestine

Brush borders and plasma membranes have been purified from mucosal epithelial cells of rabbit ileum under control conditions and after treatment for 3 hr with cholera toxin in vivo. The activity of several enzymes in these preparations was measured. It was concluded that adenyl cyclase, like NaK-ATPase, seems not to be a normal constituent of brush borders. Both these enzymes are present in plasma membrane preparations derived largely from the basal and lateral margins of the epithelial cells, both may be phospholipid dependent enzymes and both are affected by cholera toxin. Adenyl cyclase activity is increased while NaK-ATPase is decreased. The activities of alkaline phosphatase, leucineaminopeptidase, 5'-nucleotidase, glucose-6-phosphatase, and Mg-ATPase were not found to be affected by the toxin. Cholera toxin, which makes contact with the luminal side of the epithelial cells, in the natural disease and in the experimental model, would appear to exert its pathologic effect on adenyl cyclase at the opposite (basal and lateral) side of the cells.     

Renal blockade to angiotensin II in acute and chronic sodium-retaining states.

Acute thoracic inferior vena cava constriction results in alterations in renal hemodynamics which may explain the characteristic antinatriuretic response. Since adrenalvein-aldosterone secretion is increased within 30 minutes of acute caval constriction and elevated plasma-renin activity is found in the chronic caval dog, we sought to determine whether the renal hemodynamic alterations observed in acute caval constriction are due to the intrarenal action of angiotensin II. The renal response to acute caval constriction in dogs receiving unilateral renal arterial infusion of a specific competitive antagonist of angiotensin II, 1-sarcosine-8-alanine-agiotensin II, was studied. Effective blockade did not alter the renal hemodynamic or antinatriuretic response to acute caval constriction. As a model of chronic sodium retention, dogs with chronic congestive heart failure produced by tricuspid insufficiency and pulmonary stenosis were similarly studied. Effective renal blockade to antiotensin II did not affect renal hemodynamics or urinary sodium excretion. The renal hemodynamic and antinatriuretic responses to acute caval constriction and chronic congestive heart failure are not dependent on the intrarenal action of angiotensin II.