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Biomedical subjects

R B Howard

Publications and source records attributed to R B Howard.

At least 37 records · Page 2Linked to original sources
PubMed1988

Rat ovarian renin: characterization and changes during the estrous cycle.

To demonstrate the existence and help clarify the function of renin in the rat ovary, we have characterized rat ovarian renin and examined ovarian renin levels during different stages of the rat estrous cycle. We show that high concentrations of active renin are present in the rat ovary (2.9 ng angiotensin I/h/mg). Ovarian renin activity has a pH optimum of about 7.0 and is due to a glycosylated aspartyl protease with an apparent mol wt of 39,000. These properties of rat ovarian renin are identical to previously characterized rat kidney renin. In PMSG-treated immature and adult 5-day cycling rats, ovarian renin was increased about 2-fold at estrus. At all stages of the estrous cycle in the 5-day cycling rat, the ratio of active to inactive ovarian renin was about 3:1, whereas about 90% of the renin in plasma was inactive. In the hypophysectomized diethylstilbestrol-treated rat ovary, over 90% of active renin remained in the residual ovary after the granulosa cells had been expressed, suggesting a theca-interstitial localization for renin. These studies indicate that active renin exists in the rat ovary, that its levels are cyclically increased at estrus, and that this increase may be due to enhanced local production and activation of the renin precursor. These findings greatly strengthen the concept of a functional renin-angiotensin system in the rat ovary.

Ammonium Sulfate↗
PubMed1987

Control of human placental blood flow.

An overall scheme is proposed for the control of blood flows in both fetal and maternal circulations of the human placenta. The first part of the hypothesis is that fetoplacental vascular resistance is controlled locally by a reversible hypoxic fetoplacental vasoconstriction (HFPV) in response to reduced local maternoplacental oxygen delivery. Also suggested is humoral limitation of the extent of HFPV by substances circulating in hypoxic fetal blood. Secondly, it is hypothesized that maternoplacental vascular resistance is controlled humorally by release of hormones into maternal blood from the fetoplacental unit. Finally, it is proposed that chronic local maternoplacental ischemia associated with placental "aging" can induce an irreversible fetoplacental vasoconstriction by a mechanism different from HFPV in order to permanently shut down fetal blood flow to the area(s) affected.

Female↗
PubMed1987

Hypoxia-induced fetoplacental vasoconstriction in perfused human placental cotyledons.

Effects of maternal hypoxia on fetoplacental vascular resistance in the human placenta were investigated in an in vitro model in which single anatomic subunits (cotyledons) from term placentas were perfused at constant flow through both fetal and maternal circuits by means of a physiologic salt solution containing dextran. Acute reduction of oxygen tension in the maternal perfusate induced prompt fetoplacental vasoconstriction that recovered rapidly on restoration of oxygen to the perfusate. The response, hypoxic fetoplacental vasoconstriction, could be repeatedly demonstrated in the same cotyledon. The time course of hypoxic fetoplacental vasoconstriction was inversely related to oxygen tension of maternal arterial and maternal and fetal venous perfusates. Maternal and fetal venous perfusate pH and PCO2 did not change during the response. It is concluded that hypoxic fetoplacental vasoconstriction is triggered by decreased oxygen availability. It is suggested that hypoxic fetoplacental vasoconstriction may play a role in local regulation of human fetoplacental blood flow in vivo and may contribute to poor fetal prognosis in preeclampsia.

Female↗
PubMed1986

Pressor and depressor actions of prostanoids in the intact human fetoplacental vascular bed.

Effects of the prostanoids PGE2, PGF2 alpha, PGI2, PGE1, 6-keto-PGE1 and the PGH2 analogue U46619, on fetoplacental perfusion pressure were measured in human term placental cotyledons in which both fetal and maternal circuits were perfused at constant flow. Fetal arterial injections of bolus doses of PGE2, PGF2 alpha and U46619 caused reversible increases in fetal perfusion pressure. Pressor responses to PGF2 alpha and U46619 were dose-related, with threshold doses of less than or equal to 2 nmoles and 14 pmoles, respectively. Reversible dose-related decreases in fetoplacental perfusion pressure were elicited by fetal arterial injection of PGI2, 6-keto-PGE1 and PGE1; threshold concentrations were: PGI2 less than or equal to 10 pmoles, PGE1 less than or equal to 141 pmoles and 6-keto-PGE1 less than or equal to 270 pmoles. The potent depressor effect of PGI2 and the potent pressor effect of U46619, a TxA2 mimetic, in the intact human fetoplacental vascular bed suggest that endogenous PGI2 and TxA2 could play a role in modulating fetoplacental blood flow in the term placenta.

Alprostadil↗
PubMed1985

Conversion of angiotensin I to angiotensin II in the human foetoplacental vascular bed.

Pressor effects of angiotensin I (AI) and angiotensin II (AII) on the human foetoplacental vasculature were compared in dual-perfused term placental cotyledons in which foetoplacental perfusion pressure was monitored. Arterial injections of 1 nmol doses of AI and AII caused marked increases in perfusion pressure; the mean pressor response to AI was 92.9 +/- 5.8% (mean +/- s.e. mean) of the AII response. The angiotensin-converting enzyme inhibitor captopril at 2.2 microM reversibly reduced the AI response to 13.7 +/- 3.2% (mean +/- s.e. mean) of the AII response, which was unaffected. Saralasin, an AII receptor blocker, at 94 nM reversibly antagonized both AI-and AII-induced increases in foetoplacental perfusion pressure. It is concluded that foetoplacental vasoconstriction elicited by AI is due to its conversion to AII by angiotensin-converting enzyme present in the foetoplacental bed.

Angiotensin I↗