Systemic and regional hemodynamics in patients with salt-sensitive hypertension.

Abstract

Twenty-two patients with normal plasma renln and essential hypertension were classified as "salt-sensitive" (SS) (n=9) or "non-salt-sensitive" (NSS) (n=13) from an increase in mean blood pressure with changes in sodium intake from 25 to 250 meq/day. With the high sodium diet, the SS patients gained more weight (/?<0.05), retained more sodium (/><0.05), and had a greater increase in cardiac output (/?<0.05). Despite the markedly increased cardiac output, systemic vascular resistance did not change with sodium loads in the SS patients, whereas the NSS patients had a significant decrease in systemic vascular resistance. Thus, the greater increase in blood pressure with sodium loads in SS patients can be attributed not only to an increase in cardiac output, possibly resulting from greater sodium retention, but also to inappropriately elevated systemic vascular resistance. Concomitant with a greater increase in cardiac output, the SS patients had a greater increase in forearm blood flow with sodium loading than the NSS patients (p<0.02). In contrast, blood flow to the kidney and the liver was not significantly changed in either group; renal (p<0.05) and hepatic (/><0.01) vascular resistance increased significantly in SS patients but remained unchanged in NSS patients. Thus, evidence presented suggests that the greater increase in blood pressure with sodium loads seems to be characterized by a very inhomogenous distribution of local flow and resistance in SS patients; renal and hepatic blood flow remains essentially unchanged and skeletal muscle blood flow receives almost all of the increase in cardiac output Moreover, systemic vascular resistance changes did not reflect the resistance of individual beds because vasoconstriction appeared in the kidney and the splanchnic area but was masked by prominent vasodilation in the skeletal muscle. Because this hemodynamic pattern is similar to the pattern evoked during defense reaction, it is suggested that sympathetic overactivity on a selective basis might be involved in the impaired renal function for sodium excretion and the increase in blood pressure with sodium loads in SS patients. (Hypertension 1990,16:235-244)

Rationale and design of the Eplerenone combination Versus conventional Agents to Lower blood pressure on Urinary Antialbuminuric Treatment Effect (EVALUATE) trial: a double-blinded randomized placebo-controlled trial to evaluate the antialbuminuric effects of an aldosterone blocker in hypertensive patients with albuminuria

“…6,[20][21][22][23][24] Second, hyperkalemia may occur less frequently in patients with a high salt diet than a low salt diet, because salt loading decreases serum K level. 33 Moreover, animal studies, including our own, 34,35 suggest that a mild increase in serum K level may promote organ protection in relatively K-depleted CKD patients with a high salt intake.…”

Hypertension in Acromegaly: Hereditary Hypertensive Factor Produces Hypertension by Enhancing IGF-I Production.

“…a family history of hypertension as a possible participant since essential hypertension, salt-sensitive hypertension and glucocorticoid-remediable hypertension are thought to be inherited [29][30][31][32][33]. Seventy-five percent of HT patients have a family history of hypertension.…”

Renal mechanisms of salt-sensitive hypertension: contribution of two steroid receptor-associated pathways

“…A growing body of evidence indicates that excitation of the SNS underlies salt-sensitive hypertension (9,31,32,36). Salt loading increases sympathetic activity in the kidney as well as the brain, and those excitations seem to be linked, as described in detail below.…”