Control of vascular Reactivity in Pregnancy

Gant, Norman F.; Whalley, Peggy J.; Everett, Royice B.; Worley, R. J.; MacDonald, Paul C.

doi:10.1016/s0272-6386(87)80126-9

Cited by 77 publications

(40 citation statements)

References 9 publications

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“…A change in adrenal sensitivity to endogenous angiotensin II (AngII) could explain the greater Aldo response during pregnancy. For the vasculature, pregnancy has been shown to be a state of relative AngII insensitivity (17,31,32). However, a dissociation of vascular and adrenal responsiveness to AngII has been observed to occur in non-pregnant subjects on a low-salt diet (33).…”

Section: Discussionmentioning

confidence: 99%

The Renin-Aldosterone Response to Stimulation and Suppression During Normal Pregnancy

Bentley‐Lewis

Graves

Seely

2005

Hypertension in Pregnancy

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Objective-During normal pregnancy, studies have shown increased activity of the reninangiotensin-aldosterone system (RAAS) and a dissociation of plasma renin activity (PRA) and aldosterone (Aldo) evidenced by a greater increase in Aldo relative to PRA. The aims of this study were to examine the RAAS response to stimulation by upright posture and suppression by saline infusion and to investigate the PRA-Aldo dissociation under these two conditions. Methods-We studied 24 healthy normotensive women (mean ± standard error of mean, ages 29 ± 1 yrs) in sodium (Na) balance in the second and third trimesters and postpartum. Subjects underwent a 24-hour urine collection which was analyzed for Na, norepinephrine (NE), epinephrine (Epi), and dopamine (DA); a posture study with analysis of blood pressure (BP), PRA, Aldo, NE, Epi, DA, and cortisol; and a 0.9% NaCl infusion study (500 mL/hr for 3 hrs) with analysis of BP, PRA, Aldo, cortisol, and digitalis-like factor (DLF). Analyses included paired t tests to compare posture and saline responses, repeated measures to compare across periods, and percent change to evaluate the PRA-Aldo dissociation.Results-During pregnancy, PRA, Aldo, BP, catecholamines, and cortisol levels were significantly greater in upright than left lateral decubitus (LLD) posture, and the percent change in Aldo was significantly greater than the percent change in PRA. During pregnancy in response to saline infusion, BP did not change; the PRA and Aldo significantly decreased; the percent change in Aldo was significantly greater than the percent change in PRA in the second trimester; and serum DLF and cortisol levels significantly decreased.Conclusions-In longitudinally studied normal pregnancy, PRA and Aldo levels were dissociated at baseline, with stimulation and, to a lesser degree, with suppression. Norepinephrine, adrenocorticotrophic hormone, and DLF may contribute to this dissociation, and clarification of these interactions may provide insight into the regulation of aldosterone during normal and hypertensive pregnancy.

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Section: Discussionmentioning

confidence: 99%

The Renin-Aldosterone Response to Stimulation and Suppression During Normal Pregnancy

Bentley‐Lewis

Graves

Seely

2005

Hypertension in Pregnancy

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“…Considerable data implicate increases in relaxin and nitric oxide (NO) in the systemic vasodilation induced by pregnancy (20,127,128,177,196). In addition, peripheral vascular sensitivity to circulating vasoconstrictors including vasopressin, angiotensin II (ANG II), and norepinephrine (NE) is decreased (50,71,154).Unlike the hemodynamic changes, which likely subserve adequate fetal development, an adverse consequence of normal pregnancy is a marked impairment of the arterial baroreceptor reflex. This change was first noted by Humphreys and Joels (97,98) in an extensive series of studies in anesthetized pregnant rabbits, in which reductions in carotid sinus pressure failed to elicit normal increases in arterial pressure and peripheral vascular resistance.…”

mentioning

confidence: 99%

Pregnancy and the endocrine regulation of the baroreceptor reflex

Brooks

Dampney

Heesch

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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-The purpose of this review is to delineate the general features of endocrine regulation of the baroreceptor reflex, as well as specific contributions during pregnancy. In contrast to the programmed changes in baroreflex function that occur in situations initiated by central command (e.g., exercise or stress), the complex endocrine milieu often associated with physiological and pathophysiological states can influence the central baroreflex neuronal circuitry via multiple sites and mechanisms, thereby producing varied changes in baroreflex function. During pregnancy, baroreflex gain is markedly attenuated, and at least two hormonal mechanisms contribute, each at different brain sites: increased levels of the neurosteroid 3␣-hydroxydihydroprogesterone (3␣-OH-DHP), acting in the rostral ventrolateral medulla (RVLM), and reduced actions of insulin in the forebrain. 3␣-OH-DHP appears to potentiate baroreflex-independent GABAergic inhibition of premotor neurons in the RVLM, which decreases the range of sympathetic nerve activity that can be elicited by changes in arterial pressure. In contrast, reductions in the levels or actions of insulin in the brain blunt baroreflex efferent responses to increments or decrements in arterial pressure. Although plasma levels of angiotensin II are increased in pregnancy, this is not responsible for the reduction in baroreflex gain, although it may contribute to the increased level of sympathetic nerve activity in this condition. How these different hormonal effects are integrated within the brain, as well as possible interactions with additional potential neuromodulators that influence baroreflex function during pregnancy and other physiological and pathophysiological states, remains to be clearly delineated.3␣-hydroxy-dihydroprogesterone; angiotensin II; insulin; paraventricular nucleus of the hypothalamus NORMAL PREGNANCY is characterized by profound changes in fluid and electrolyte balance and blood pressure regulation. Blood volume and cardiac output increase by 30 -50%, but arterial pressure falls due to even greater decreases in systemic vascular resistance (120,138,189). These hemodynamic alterations are evident early in pregnancy, precede the increases in uterine blood flow, and are sustained until parturition (127,138,189). Considerable data implicate increases in relaxin and nitric oxide (NO) in the systemic vasodilation induced by pregnancy (20,127,128,177,196). In addition, peripheral vascular sensitivity to circulating vasoconstrictors including vasopressin, angiotensin II (ANG II), and norepinephrine (NE) is decreased (50,71,154).Unlike the hemodynamic changes, which likely subserve adequate fetal development, an adverse consequence of normal pregnancy is a marked impairment of the arterial baroreceptor reflex. This change was first noted by Humphreys and Joels (97,98) in an extensive series of studies in anesthetized pregnant rabbits, in which reductions in carotid sinus pressure failed to elicit normal increases in arterial pressure and peripheral vascular resistanc...

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“…It can be speculated that in preeclampsia the changes in absolute concentrations of 6-keto-PGFIa and TXB2 are less important than the decrease in the ratio of the 6-keto-PGFIa/TXB2. plasma renin activity ; angiotensin II ; prostacyclin ; tromboxane A2; preeclampsia The renin-angiotensin system is known to play an important role in the maintenance of normal blood pressure and it has been shown that women who have, or are destined to develop, preeclampsia show an increased sensitivity to infused angiotensin II (Gant et al 1976). This effect can be abolished by the administration of prostaglandin E2 or induced by the prior administration of an inhibitor of prostaglandin synthetase (Everetta et al 1978).…”

mentioning

confidence: 99%

“…The renin-angiotensin system is known to play an important role in the maintenance of normal blood pressure and it has been shown that women who have, or are destined to develop, preeclampsia show an increased sensitivity to infused angiotensin II (Gant et al 1976). This effect can be abolished by the administration of prostaglandin E2 or induced by the prior administration of an inhibitor of prostaglandin synthetase (Everetta et al 1978).…”

mentioning

confidence: 99%

Plasma renin activity, angiotensin II, prostacyclin and thromboxane A2 concentrations in 139 preeclamptic patients.

Furuhashi¹,

Tsujiei²,

Kimura³

et al. 1990

Tohoku J. Exp. Med.

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Plasma renin activity , plasma concentratrions of angiotensin 11(AngII), stable metabolites (6-keto-prostaglandin Fla : 6-keto-PGFIa) of prostacyclin (PGI2) and a metabolite (thromboxane B2: TXB2) of thromboxane A2 (TXA2 ) were measured with radioimmunoassay(RIA) in 107 normal pregnancy (control) and 139 preeclamptic patients in 28-41 gestational weeks. PRA and 6-ketoPGFIa were significantly higher and AngII was slightly higher in preeclampsia than in control, and TXB2 was significantly lower in preeclampsia in control. The ratio of 6-keto-PGFIa/TXB2 was significantly lower in preeclampsia than in control. These data suggest that the changes in the renin-angiotensin system may not be primary alterations in preeclampsia. It can be speculated that in preeclampsia the changes in absolute concentrations of 6-keto-PGFIa and TXB2 are less important than the decrease in the ratio of the 6-keto-PGFIa/TXB2. plasma renin activity ; angiotensin II ; prostacyclin ; tromboxane A2; preeclampsia The renin-angiotensin system is known to play an important role in the maintenance of normal blood pressure and it has been shown that women who have, or are destined to develop, preeclampsia show an increased sensitivity to infused angiotensin II (Gant et al. 1976). This effect can be abolished by the administration of prostaglandin E2 or induced by the prior administration of an inhibitor of prostaglandin synthetase (Everetta et al. 1978). It is well established that vasocon-striction in the arteriolar bed, particularly in the uterus and kidney, is a characteristic feature of preeclampsia. Thromboxane A2 (TXA2) and prostacyclin (PGI2) are potent vasoactive compounds. TXA2 causes vasoconstriction and induces platelet aggregation, whereas PGI2 has the opposite properties (Moncada and Vane 1978). Other studies with isolated tissues have shown that there

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Control of vascular Reactivity in Pregnancy

Cited by 77 publications

References 9 publications

The Renin-Aldosterone Response to Stimulation and Suppression During Normal Pregnancy

The Renin-Aldosterone Response to Stimulation and Suppression During Normal Pregnancy

Pregnancy and the endocrine regulation of the baroreceptor reflex

Plasma renin activity, angiotensin II, prostacyclin and thromboxane A2 concentrations in 139 preeclamptic patients.

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