Hormones and hemodynamics in pregnancy

Abstract

Context: Normal pregnancy is associated with sodium and water retention, which results in plasma volume expansion prior to placental implantation. The explanation offered for these events is that pregnancy 'resets' both volume and osmoreceptors.

Evidence acquisition: The mechanisms for such an enigmatic 'resetting' in pregnancy have not previously been explained. However, recent human pregnancy studies have demonstrated that the earliest hemodynamic change in pregnancy is primary systemic arterial vasodilation. This arterial underfilling is associated with a secondary increase in cardiac output and activation of the neurohumoral axis, including stimulation of the renin-angiotensin-aldosterone, sympathetic, and non-osmotic vasopressin systems. Resistance to the pressor effects of angiotensin and sympathetic stimulation in pregnancy is compatible with an increase in endothelial nitric oxide synthase activity.

Results: In contrast to the sodium and water retention which occur secondary to the primary arterial vasodilation in cirrhosis, glomerular filtration and renal blood flow are significantly increased in normal pregnancy. A possible explanation for this difference in arterial vasodilation states is that relaxin, an arterial vasodilator which increases during pregnancy, has a potent effect on both systemic and renal circulation. Endothelial damage in pregnancy is pivotal in the pathogenesis of preeclampsia in pregnancy.

Conclusions: Against a background of the primary arterial vasodilation hypothesis, it is obvious that reversal of the systemic vasodilatation in pregnancy, without subsequent activation of the renin-angiotensin-aldosterone system (78), will evoke a reversal of all the links in the chain of events in normal pregnancy adaptation, thus, it may cause preeclampsia. Namely, a decrease of renal vasodilation will decrease glomerular filtration rate.

Keywords: Arterial; Nitric Oxide; Osmolar Concentration; Pre-Eclampsia, Endothelium; Pregnancy; Relaxin.

Figures

Figure 1.. Body Fluid Regulation in Health and Disease: A Unifying Hypothesis., Renin-Angiotensin-Aldosterone System (RAAS); Sympathetic Nervous System (SNS). Reproduced with Permission from Ref. .

Figure 2.. Ten Women Studied in the Mid-Follicular Phase of the Menstrual Cycle and Weeks 6, 8, 10, 12, 24 and 36 Gestation. Reproduced with Permission from Ref. .

A. Systemic hemodynamic changes throughout early human pregnancy. Mean arterial pressure (MAP) decreased and cardiac output (CO) increased significantly by week 6 gestation in association with a decrease in systemic vascular resistance (SVR). *P

Figure 3.. Ten Women Were Studied in the Mid-Follicular Phase of the Menstrual Cycle and Weeks 6, 8, 10, 12, 24 and 36 Gestation Reproduced With Permission From Ref.

A. Renal hemodynamic changes throughout early human pregnancy. Renal plasma flow and glomerular filtration rates increased significantly in association with a renal vascular resistance by week 6 gestation. Twenty-four-hour urinary creatinine excretion remained unchanged throughout gestation. Abbreviations: CIn, inulin clearance; CPAH, para-aminohippurate clearance; RVR, renal vascular resistance; UCrV, urinary creatinine excretion. *P

Figure 4.. Hypoosmolality in Pregnancy (A) Associated with Increased Plasma Arginine Vasopressin (AVP) (B) and a Rise in Hypothalamic AVP (C).

Figure 5.. Chronic Nitric Oxide Synthase (NOS) Inhibition Returns Cardiac Output (CO) and Systemic Vascular Resistance (SVR) in Day 14 Pregnant Rats to Nonpregnant Levels.

Values are means + /- SE for CO (A), and calculated SVR (A). *P