In severe heart failure associated with cardiomyopathy, norepinephrine uptake is reduced. In addition, myocardial adrenergic nerve activity is accelerated in proportion to severity of heart failure, independent of the underlying cause.

SUMMARY. The study was performed to determine whether there is a structural vascular abnormality in normotensive subjects with hypertensive relatives. We examined maximal vasodilator capacity of forearm resistance vessels in 23 normotensive young men (mean blood pressure 94 ± 0.4 mm Hg, mean ± SE) with hypertensive relatives (age 24 ± 0.1 years) and in 17 normotensive subjects (mean blood pressure 85 ± 0.4 mm Hg) with no family history of hypertension (age 24 ± 0.1 years). Maximal vasodilator capacity was examined by measuring minimal vascular resistance during peak reactive hyperemia after release from 10 minutes of arterial occlusion. Minimal forearm vascular resistance after release from 10 minutes of arterial occlusion was 25% higher (P < O.02) in subjects with hypertensive relatives (2.0 ± 0.02 units) than that in subjects with no family history (1.5 ± 0.01 units). We confirmed the previous findings that increasing metabolic vasodilator stimulus by performing intermittent handgrip exercise during 10 minutes of arterial occlusion did not augment peak dilation. This suggests that 10 minutes of arterial occlusion produced maximal vasodilation. Forearm vascular responses to ice on the forehead was greater in subjects with hypertensive relatives than those in subjects with no family history. These results suggest that there may be a structural abnormality in the forearm resistance vessels in normotensive subjects with family history of hypertension. (Circ Res 50: 671-677, 1982)

In heart failure due to mitral stenosis, myocardial adrenergic nerve activity is intensified. A decrease in cardiac output associated with mitral stenosis acts as a potent stimulus for this intensification.

No abstract

It has been previously suggested that salt loading produces structural changes of the arteries in hypertensive patients who respond to salt loading with a greater rise of blood pressure. This study examined the possibility that salt loading alters venous distensibility in hypertensive patients. Twenty-one patients with essential hypertension were placed on a low-sodium diet (70 meq) for 7 days and then were placed on a high-sodium diet (345 meq) for 7 days. Patients were arbitrarily divided into two groups based on the response of their blood pressure to salt loading: (1) those whose mean blood pressure increased by more than 10% while on the high-salt diet as compared with those on the low-salt diet (salt-responsive patients, n = 8) and (2) those whose mean blood pressure did not increase by more than 10% (salt-nonresponsive patients, n = 13). The venous pressure-volume relationship was determined in the forearm with a water-filled plethysmograph when patients were on the low-and high-salt diet. Venous pressure-volume curves were not different between salt-responsive and salt-nonresponsive patients while on the low-salt diet. High-salt intake shifted the curve toward the pressure axis for salt-responsive patients (p < .05) but not for salt-nonresponsive patients. Phentolamine, 1 mg administered intravenously for 5 min, did not significantly alter venous pressure-volume curves for either group while on the low-or high-salt diet. These results suggest that salt loading decreased venous distensibility in salt-responsive patients, which resulted from nonadrenergic mechanisms: structural changes of the veins could perhaps be included as one of these mechanisms. Circulation 69, No. 1, 50-56, 1984. EPIDEMIOLOGIC STUDIES suggest that an excessive intake of salt contributes to the prevalence of essential hypertension in humans.' However, the mechanisms by which an excessive intake of salt promotes hypertension in humans are not clear.Recent