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N F Gant

Publications and source records attributed to N F Gant.

81 records · Page 5Linked to original sources
PubMed1973

A study of angiotensin II pressor response throughout primigravid pregnancy.

The present study was designed to ascertain sequentially the pressor response to angiotensin II in young primigravid patients throughout pregnancy in order a) to define when in pregnancy resistance to the pressor effects of angiotensin II develops; b) to define the physiologic sequence of events leading to this resistance; and c) to ascertain whether sensitivity to infused angiotensin II could be detected before the onset of clinical signs of pregnancy-induced hypertension. With this prospective approach, two separate groups of patients were defined. The first group of patients remained normal throughout pregnancy. The second group consisted of those patients who, while clinically normotensive during the initial phase of the study, ultimately developed hypertension of pregnancy.192 patients were studied; of these, 120 patients remained normotensive and 72 developed pregnancy-induced hypertension. In both groups, vascular resistance to infused angiotensin II (more than 8 ng/kg/min required to elicit a pressor response of 20 mm Hg in diastolic pressure) was demonstrated as early as the 10th wk of pregnancy. In the group that remained normotensive, maximum mean vascular resistance occurred at 18-30 wk of pregnancy, (mean pressor dose required being 13.5 to 14.9 ng/kg/min). In those subjects who developed pregnancy-induced hypertension, the mean maximum dose required was 12.9 ng/kg/min, which was observed at the 18th wk of pregnancy. By the 22nd wk there was a clear separation of the two groups, with the mean dose requirement of the subjects destined to develop hypertension being progressively less than that of those who remained normal. The difference between the two groups became significant (P < 0.01) by 23-26 wk of pregnancy. Among patients requiring more than 8 ng/kg/min on one or more tests done between wk 28-32, 91% remained normotensive. Conversely, during the same time period among patients requiring less than 8 ng/kg/min, on at least one occasion, 90% developed pregnancy-induced hypertension.

Adolescent↗
PubMedDate not supplied

Partial characterization of guanylate cyclase activity of the human placenta.

An optimal assay system for the measurement of GC activity in subcellular fractions of human placenta homogenates was developed. MN2+ was more effective than Mg2+ as a cofactor and, in addition, it markedly potentiated the Mg2+-dependent GC activity. The apparent optimal temperature for GC activity was 45 degrees C and the pH optimum was in the range of 7.5 to 8.3. The apparent Km of Mn2+-dependent GC for GTP was 0.1 and that of MG2+-dependent GC for GTP was 0.4 mm. More than 95 per cent of GC activity was associated with the 100 000 X g supernatant fraction. ATP at a concentration of 0.5 mm inhibited GC activity by 50 per cent. The Mn2+-dependent GC activity was inhibited by p-hydroxymercuriphenyl sulphonate at concentrations between 10 and 50 micrometers; this inhibition was reversed, in part, by dithiothreitol at concentrations of 150 to 500 micrometers to approximately one-fifth the activity of control values. In addition, we found that dithiothreitol was an inhibitor of GC activity. Studies on the responsiveness of placental GC to nucleophilic compounds indicated that phenylhydrazine was the most potent stimulus, while hydroxylamine, hydrazine, sodium azide, sodium nitrite and sodium nitroprusside were less potent. Placental GC was unaffected by alpha- and beta-adrenergic agonists or by cholinergic agonist, as well as by steroids produced by the placenta.

Cyclic GMP↗
PubMedDate not supplied

Adenylate cyclase from term human placenta and its regulation.

The activation of placental AC by either Mg2+ or Mn2+, in the presence and absence of NaF, followed sigmoidal saturation kinetics. Mn2+ enhanced maximally the NaF-stimulated Mg2+-dependent AC activity. The apparent Km of Mg2+-dependent AC for ATP was 0.4 mM, with and without NaF addition. GTP and GMP-P(NH)P stimulated the Mg2+-dependent AC in a dose-dependent manner with half-maximal stimulation taking place at concentrations of approximately 2 microM. In the presence of GMP-P(NH)P (10 microM) the kinetics of the AC dependence on Mg2+ ion concentration changed from sigmoidal to hyperbolic. Most of the AC activity (greater than 83 per cent) was associated with the particulate fractions of placental homogenate. For better reproducibility, the AC assay was performed using sonicated particulate fraction preparations; sonication did not alter the response of AC to stimuli to a variety of agents used in these experiments; freezing and thawing, however, obliterated the stimulation by beta-adrenergic agonists. Placental AC activity was inhibited by p-hydroxymercuriphenyl sodium sulphonate in a dose-dependent fashion, and the inhibition was reversed by dithiothreitol. Mg2+-dependent AC was inhibited by 0.5 mM phenylhydrazine (95 per cent). Mg2+-dependent AC activity was responsive to stimulation by epinephrine, without and with GTP addition, with half-maximal stimulation taking place at a concentration of 2 microM. The stimulatory effect of epinephrine was blocked by propranolol in a dose-dependent manner but was not blocked by phentolamine. Oestrone, oestradiol-17 beta, 2-hydroxyoestreone, 2-hydroxyoestradiol-17 beta, dehydroepiandrosterone sulphate, and progesterone, as well as oxytocin, did not alter either the basal or GMP-P(NH)P-stimulated Mg2+-dependent AC activities. Preincubation of 20 000 g particulate fraction with either NaF or GMP-P(NH)P, followed by washing, resulted in preparations that remained stimulated without the requirement of any further additions.

Adenylyl Cyclases↗