Studies on etiology of essential hypertension. Hemodynamics, water-sodium balance and response to pressor substances during long-term sodium restriction and after spontaneous blood pressure fall--.
CI, TPRI, PV, ECFV, Nae, PRA and a pressor response to NA and AT was measured before and after 1) sodium restriction and 2) spontaneous blood pressure fall (spontaneous fall) in the patients with essential hypertension and the following results were obtained. 1) CI did not change during sodium restriction and increased after spontaneous fall. TPRI was reduced and the degree of this reduction was positively correlated with that of blood pressure reduction under these two conditions. 2) Sodium restriction caused the decrease of PV, ECFV and Nae and the increase of PRA. The degree of the reduction of PV and Nae was positively correlated with that of blood pressure fall. After spontaneous fall, PV, ECFV and NAe  was increased and PRA did not change significantly. 3) A pressor response to NA and AT was depressed after one week of sodium restriction, and after 4 weeks the former returned to the basal response, while the latter was still reduced. NA response was correlated positively with basal Nae, ECFV and interstitielle fluid volume and negatively with basal PRA. AT response was negatively correlated with PRA before and during sodium restriction. No correlation was  observed, however, between the degree of reduction of blood pressure and that of the change in pressor response to NA or AT. After spontaneous fall, the response to NA was not reduced but increased. These results suggested that, although the fall in blood pressure under these experimental conditions was mediated by the reduction of TPRI, the changes in pressor response to NA and AT did not affect primarily the reduction of blood pressure.
D000804:Angiotensin II / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects*; D004039:Diet, Sodium-Restricted; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D006584:Hexamethonium Compounds / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D007273:Injections, Intramuscular; D009638:Norepinephrine / Q000494:pharmacology; D010953:Plasma Volume; D011188:Potassium / Q000378:metabolism; D011863:Radioimmunoassay; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism*; D014655:Vascular Resistance
D006584:Hexamethonium Compounds; D000804:Angiotensin II; D012964:Sodium; D012083:Renin; D011188:Potassium; D009638:Norepinephrine