Calf muscle haemodynamics and the renin-angiotensin-aldosterone system in normotensive subjects with a familial predisposition to hypertension: changes during increased salt intake.
Blood pressure, plethysmographically determined muscle blood flow in the calf at rest and during maximal dilatation, plasma renin activity, angiotensin II and plasma and urinary aldosterone were determined in normotensive men with a positive family history of hypertension (n = 17) and in an age- and weight-matched control group (n = 15) during usual sodium intake and after four weeks of increased salt intake. On normal salt intake resting muscle blood flow was significantly lower and resting resistance and resting vascular tone significantly higher in those with a positive family history, reflecting a stronger smooth muscle contraction of the resistance vessels in the calf at rest. Flow and resistance at maximal dilatation did not differ between the groups, indicating no difference in the structural design of the resistance vessels in the calf. Plasma angiotensin II and urinary aldosterone were not significantly different between the two groups. Plasma renin activity was, however, significantly higher in those with a positive family history which might be interpreted as increased renal sympathetic activity in the genetically predisposed subjects. After four weeks of increased salt intake no significant changes were noted in blood pressure, muscle blood flow and resistance at rest or at maximal dilatation in either of the two groups. Plasma renin activity and angiotensin II decreased significantly in both groups after 10 days of increased salt but tended to return to normal values at the end of the fourth week. Plasma aldosterone and urinary aldosterone excretion were equally and significantly decreased in both groups giving no evidence for an inadequate suppression of aldosterone in subjects genetically predisposed to hypertension.
D000293:Adolescent; D000328:Adult; D000450:Aldosterone / Q000097:blood / Q000652:urine; D000804:Angiotensin II / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D007866:Leg / Q000098:blood supply / Q000502:physiology; D008297:Male; D009132:Muscles / Q000098:blood supply* / Q000502:physiology; D012039:Regional Blood Flow / Q000187:drug effects; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System; D012965:Sodium Chloride / Q000494:pharmacology*; D014655:Vascular Resistance / Q000187:drug effects
D000804:Angiotensin II; D012965:Sodium Chloride; D000450:Aldosterone; D012083:Renin