Seasonal variation in blood pressure (BP) has been described in some people, although the variation is small for both systolic and diastolic BPs. The aim of this study was to elucidate underlying haemodynamic and hormonal mechanisms that may occur to defend seasonal changes in BP. Participants were 27 men and 7 women with either normal BP or early hypertension. Measurements of haemodynamics (cardiac output by dual-gas rebreathing) and hormones (resting catecholamines, renin activity, and aldosterone by radioenzymatic assay or radioimmunoassay) were performed during the summer, fall, winter, and spring seasons. Student's paired t-test with Bonferroni modification and regression analyses were used to examine the data with a significance level of Po0.05. Systolic and diastolic BP remained relatively constant across seasons. Cardiac output and stroke volume significantly decreased 10 and 15%, respectively, from summer to winter, whereas heart rate and systemic vascular resistance significantly increased 5 and 11%, respectively. Plasma aldosterone (PA) significantly increased 59% from summer to winter, whereas plasma norepinephrine (PNE), plasma epinephrine, and plasma renin activity (PRA) increased 19, 2, and 17%, respectively (pNS for each). Across the four seasons, mean arterial pressure significantly correlated with PRA and PA, whereas systemic vascular resistance significantly correlated with PNE and PRA. There are dramatic counterregulatory haemodynamic and hormonal adaptations to maintain a relatively constant BP. Norepinephrine, PRA, and aldosterone have a function in mediating the changes in haemodynamics.
Small changes in sodium concentration [( Na]) are not generally considered to have a major direct effect on aldosterone secretion. However, a marked disruption in the renin-aldosterone relationship has been observed in a variety of hypernatremic and hyponatremic states. Therefore, we evaluated the hypothesis that small changes in [Na] have a potent direct effect on angiotensin II- and potassium-stimulated aldosterone secretion. The left adrenal gland, abdominal aorta, and surrounding periadrenal tissue were surgically isolated from mongrel dogs and perfused with Ringers bicarbonate solution at a pressure of approximately 57 mm Hg. Infusion of a KCl test solution at the beginning and end of most experiments produced similar increases in aldosterone secretion, thus documenting the stability of these preparations. After a stable response was established to either a low dose of angiotensin II or a small increase in perfusate [K], the [Na] was changed by adding or removing NaCl. Changing perfusate [Na] from 152 to 139 mM during the infusion of either angiotensin II or potassium caused 20- to 25-fold increases in aldosterone secretion. Increasing perfusate [Na] from 145 to 152 mM inhibited aldosterone secretion to a greater extent during stimulation by lower doses (40-50 pg/ml) than by higher doses (80-100 pg/ml) of angiotensin II. These data demonstrate that during moderate stimulation by angiotensin II or potassium, small changes in [Na] have a powerful inverse effect on aldosterone secretion by a direct action on the canine adrenal gland.
The purpose of these experiments was to determine if the powerful effect of sodium chloride concentration on angiotensin II- and potassium-stimulated aldosterone secretion by isolated perfused adrenal glands is mediated by the sodium or chloride ion or by the obligatory change in osmolality. We used isolated Ringer's bicarbonate perfused canine adrenal gland preparations to determine the effects of a variety of isosmotic, hyperosmotic, and hyposmotic solutions on angiotensin II- and potassium-stimulated aldosterone secretion. When we increased the osmolality of the perfusion medium (8-10 mosmol) by the addition of NaCl, sucrose, mannitol, or glucose, angiotensin II-stimulated aldosterone secretion was inhibited to a similar extent, whereas urea addition had no effect. Similarly, when we increased the osmolality of the perfusion medium (8-10 mosmol) by the addition of NaCl, sucrose, or mannitol, potassium-stimulated aldosterone secretion was also inhibited to a similar extent. In contrast to the increase in angiotensin II- and potassium-stimulated aldosterone secretion observed during hyposmotic reductions in NaCl concentration, (addition of sucrose) did not increase angiotensin II- or potassium-stimulated aldosterone secretion. Even the marked increase in aldosterone secretion caused by large hyposmotic reduction in NaCl concentration did not occur with an equivalent isosmotic reduction in NaCl concentration. These results clearly demonstrate that changes in NaCl concentration affect aldosterone secretion by a mechanism sensitive to the osmolality. Moreover, since hyperosmolality caused by urea addition had no effect on angiotensin II-stimulated aldosterone secretion, changes in intracellular volume or composition appear to be an important modulator of aldosterone secretion.
The functional role of H1 and H2 receptors in mediating the effects of histamine on renal hemodynamics and tubular function was investigated in anesthetized dogs. Histamine, infused directly into the renal artery, caused decreases in renal vascular resistance and increases in total renal blood flow without significant changes in mean arterial blood pressure or glomerular filtration rate. These hemodynamic effects of histamine were inhibited by the H2-receptor antagonist, cimetidine, but not by the H1-receptor antagonist, tripelennamine. Histamine also caused increases in fractional urine flow and the fractional excretion of sodium and calcium with a concomitant decrease in urine/plasma osmolality. These tubular effects of histamine were antagonized by both tripelennamine and cimetidine. Histamine-induced increases in the fractional excretion of potassium were blocked only by tripelennamine. These results suggest that (1) both H1 and H2 receptors mediate the effects of histamine on urinary dilution and tubular reabsorption; (2) H2 receptors mediate the effects of histamine on renal hemodynamics, indicating that H2 receptors are present in the renal vasculature, and (3) H1 receptors may exist in the renal tubules.
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