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Showing papers by "Suzanne Oparil published in 1985"


Journal ArticleDOI
TL;DR: Imposition of increased loads on the hearts of older animals results in cardiac hypertrophy due to enlargement of myocardial cells and hyperplasia of nonmuscular components, which results in growth of the vertebrate heart during embryonic and fetal life.

69 citations


Journal ArticleDOI
01 Nov 1985-Peptides
TL;DR: Amperometric detection of oxidizable amino acids in the peptide sequence of a number of endogenous neuropeptides proved suitable for the identification of peptide standards and quantification of neural lobe arginine vasopressin and striatal methionine enkephalin.

17 citations


Journal ArticleDOI
TL;DR: The hyperprolactinemia and enhanced depressor response to bromocriptine observed in DOCA/NaCl animals suggest that the dopaminergic system might be altered in this model of hypertension.
Abstract: To elucidate the role of the dopaminergic system in the maintenance of hypertension in the deoxycorticosterone acetate (DOCA)/NaCl hypertensive rat, the responses of mean arterial pressure (MAP), plasma norepinephrine (NE), epinephrine (E), and prolactin (PRL) to intravenous (iv) administration of bromocriptine, a dopamine agonist, and hexamethonium bromide, a ganglion blocker, were examined in conscious, unrestrained 4-wk DOCA/NaCl hypertensive rats. Bromocriptine was administered to adrenomedullectomized (ADMX) rats to assess the role of the adrenal medulla in its depressor effect. Bromocriptine (50, 250, and 500 micrograms/kg) and hexamethonium (3 and 30 mg/kg) caused dose-dependent decreases in MAP that were greater in DOCA/NaCl rats than in uninephrectomized controls. Basal plasma NE, E, and PRL were significantly higher in DOCA/NaCl rats than in controls. Bromocriptine (500 micrograms/kg iv) decreased plasma PRL to undetectable levels and increased plasma E significantly without changing NE levels in DOCA/NaCl and uninephrectomized control rats. In ADMX rats bromocriptine (500 micrograms/kg iv) decreased MAP, PRL, and NE without affecting E levels. These results suggest that the depressor response to bromocriptine could be related to inhibition of sympathetic outflow without participation of the adrenal medulla. The hyperprolactinemia and enhanced depressor response to bromocriptine observed in DOCA/NaCl animals suggest that the dopaminergic system might be altered in this model of hypertension.

9 citations


Journal ArticleDOI
TL;DR: The results suggest that the activity of the central GABAergic system is altered in the rat with established DOCA/NaCl hypertension and that the alteration incentral GABAergic function may be related to the increased sympathoadrenal activity and the maintenance of hypertension in this model.
Abstract: To elucidate the role of the central gamma-aminobutyric acid (GABA) system in the maintenance of deoxycorticosterone (DOCA)NaCl hypertension, the responses of mean arterial pressure (MAP), plasma norepinephrine (NE), and epinephrine (EP) to intracerebroventricular (ICV) administration of muscimol, a GABA agonist, and the responses of MAP to bicuculline, a GABA antagonist, and to clonidine, an alpha 2-adrenoceptor agonist known to lower blood pressure by inhibiting sympathetic tone, were examined in conscious, unrestrained 4 week DOCA/NaCl hypertensive rats and age-matched uninephrectomized control rats. Muscimol (50-1000 ng/300 g, ICV) caused dose-dependent decreases in MAP which were greater in DOCA/NaCl rats than in controls. Basal plasma NE and EP were significantly higher in DOCA/NaCl rats than in controls. Muscimol (1000 ng/300 g, ICV) induced decreases in plasma EP which were greater in DOCA/NaCl rats than in controls without changing NE levels in either group. Bicuculline (3 micrograms/300 g, ICV) caused increases in MAP which were the same in both groups. The depressor response to clonidine (5 micrograms/300 g) was greater in DOCA/NaCl rats than in controls. These results suggest that the activity of the central GABAergic system is altered in the rat with established DOCA/NaCl hypertension and that the alteration in central GABAergic function may be related to the increased sympathoadrenal activity and the maintenance of hypertension in this model.

9 citations


Journal ArticleDOI
TL;DR: The results indicate that sympathetic nervous system activity increases progressively during the development ofDOCA/NaCl hypertension and that the sympathoadrenal system is hyperresponsive to environmental stress even early in the course of DOCA/ NaCl treatment and suggest that hypothalamo-hypophyseal function is altered in this model of hypertension.
Abstract: To examine the role of the sympathetic nervous system in the development of deoxycorticosterone acetate (DOCA)/NaCl hypertension and to test the hypothesis that the responsiveness of the sympathetic nervous system to stress is enhanced during the developmental phase of hypertension in this model before resting sympathetic activity becomes increased, DOCA/NaCl-treated rats and uninephrectomized control animals were studied after 3, 7, 14, and 28 days of treatment. Basal plasma norepinephrine and epinephrine in conscious, unrestrained resting DOCA/NaCl-treated rats were the same as in controls at 3, 7, and 14 days but were significantly elevated at 28 days of treatment. Ganglionic blockade resulted in a significantly greater decrease in mean arterial pressure in DOCA/NaCl rats than in controls at 14 and 28 days of treatment. At 14 days, DOCA/NaCl rats exhibited significantly greater increments in plasma norepinephrine and epinephrine following cold stress than did H2O controls. Basal plasma prolactin levels were elevated and release of dopamine from isolated superfused mediobasal hypothalami reduced in 28-day DOCA/NaCl hypertensive rats. These results indicate that sympathetic nervous system activity increases progressively during the development of DOCA/NaCl hypertension and that the sympathoadrenal system is hyperresponsive to environmental stress even early in the course of DOCA/NaCl treatment and suggest that hypothalamo-hypophyseal function is altered in this model of hypertension.

5 citations