Showing papers by "Suzanne Oparil published in 1975"
TL;DR: Progesterone failed to produce an acute increse in urinary sodium in subjects hyperexpanded by administration of exogenous mineralocorticoids, and results suggest that the acute natriuretic action of progesterone is in part independent of aldosterone inhibition and that progester one may inhibit sodium reabsorption at proximal as well as distal sites in the nephron.
Abstract: 1. The effect of progesterone on renal haemodynamics and intrarenal sodium handling was evaluated in thirteen normal men on a constant diet. Clearances were measured during maximal water diuresis and again 4–7 days later, this time 3 h after progesterone was given intramuscularly. Seven additional studies were performed 3 days after progesterone administration. Another four tests were performed on volunteers who had manifested renal ‘escape’ from the sodium-retaining effect of deoxycorticosterone acetate. 2. In acute progesterone studies glomerular filtration rate was unchanged, whereas effective renal plasma flow increased, so that filtration fraction decreased significantly. A similar increase in urinary sodium occurred whether subjects received a low or high sodium diet. Indices which related to the distal delivery of filtrate (fractional urine flow and the sum of fractional free water and sodium clearances) increased significantly in both groups. The progesterone-induced increase in sodium excretion was not related to changes in plasma renin activity, renin substrate or urinary aldosterone. After 3 days of progesterone, the increase of sodium excretion was less than in the acute studies and urinary aldosterone increased two- to four-fold. Progesterone failed to produce an acute increase in urinary sodium in subjects hyperexpanded by administration of exogenous mineralocorticoids. 3. Results suggest that the acute natriuretic action of progesterone is in part independent of aldosterone inhibition and that progesterone may inhibit sodium reabsorption at proximal as well as distal sites in the nephron.
79 citations
TL;DR: It is concluded that 6-OHDA does not produce its effect through a nonspecific lowering of blood pressure, but rather, that it interferes with the expression of the hypertensive syndrome.
Abstract: Six-hydroxydopamine (6-OHDA) was administered intraventricularly to 6-week-old male spontaneously hypertensive (SH) rats of the Okomoto strain and to normotensive rats of the Kyoto-Wistar strain. In addition, bilateral lateral tegmental lesions were placed in 35-40-day-old SH rats to interrupt ascending noradrenergic pathways. SH rats treated with 6-OHDA did not develop hypertension and had lower heart rates than control rats. Blood pressure and heart rate of Kyoto-Wistar animals were unaffected by the drug treatment. 6-OHDA produced widespread depletion of norepinephrine throughout the CNS of both SH and Kyoto-Wistar rats. Bilateral lateral tegmental lesions interrupted the dorsal noradrenergic bundle and depleted forebrain norepinephrine. These lesions did not prevent the development of hypertension and led to an increased heart rate. It is concluded that 6-OHDA does not produce its effect through a nonspecific lowering of blood pressure, but rather, that it interferes with the expression of the hypertensive syndrome. The lack of effect seen following depletion of forebrain norepinephrine as the result of interruption of the dorsal noradrenergic bundle indicates that the fibers destroyed by this lesion are not essential for the development of genetically determined hypertension.
32 citations
Journal Article•
TL;DR: Good results have been reported in those women taking OCs from the middle range, and possible risk factors increasing hypertensive susceptibility include genetic character istics preexisting and occult renal disease age and weight and possibl e antececent eclampsia.
Abstract: Although the prevalence of pill-induced or -enhanced hypertension is uncertain data have demonstrated the development of new hypertension or the acceleration of preesisting high blood pressure following administration of estrogen-containing oral contraceptives (OCs). The report incidence of hypertension ranges from 0 to 18% and 0 to 7% in patients without antecedent hypertension. Preeclampsia has a similar rate. The renin-angiotensin system is affected by estrogen which stimulates the hepatic synthesis of renin substrate. Estrogen also depresses urinary solium excretion in normal humans and directly contributes to sodium retention. Estrogen-induced changes in cardiovascular status are attributable to the hypertensive effect of the pill. Increased sympathetic activity has been postulated as a mechanism responsible for essential and pill-related hypertension. Possible risk factors increasing hypertensive susceptibility include genetic character istics preexisting and occult renal disease age and weight and possibl e antececent eclampsia. Careful examinations and complete histories pri or to and close observations during OC therapy are advised. Those who become hypertensive or have hypertensive symptoms should be with drawn from therapy. Good results have been reported in those women taking OCs from the middle range.
25 citations
TL;DR: An adaptive treatment algorithm for guiding antihypertensive drug administration has been created, and acceptability of its recommendations to consulting physicians measured.
4 citations