Maternal endothelial nitric oxide synthase genotype influences offspring blood pressure and activity in mice.

Deficiencies in maternal endothelial NO synthase (eNOS) have been associated with pregnancy complications, intrauterine growth retardation, and altered vascular function in offspring. In the present study, we investigated the influence of the maternal eNOS genotype on offspring's blood pressure, heart rate, and locomotor activity. The effect of maternal eNOS genotype was made by comparing telemetered blood pressure and activity between 2 groups of 13- to 16-week-old male heterozygous eNOS knockout mice, 1 produced by a cross of eNOS knockout (eNOS-/-) mothers and wild-type (eNOS+/+) fathers (eNOS(+/-MAT) offspring, N=11), the other by a cross of eNOS+/+ mothers and eNOS-/- fathers (eNOS(+/-PAT) offspring, N=10).

Increased salt-sensitivity in endothelial nitric oxide synthase-knockout mice.

Background: Although impaired nitric oxide production contributes importantly to salt-sensitivity, the role of the endothelial isoform of nitric oxide synthase (eNOS) has received little attention. In the present study we compared the effects of a high-salt diet on the blood pressure response of eNOS knockout (eNOS-/-) and control (eNOS+/+) mice.

Methods: Mean arterial pressure (MAP), heart rate, pulse pressure, and activity levels were recorded by telemetry in mice fed a regular-salt diet (0.

Distinct rapid and slow phases of salt-induced hypertension in Dahl salt-sensitive rats.

Objective: To test the hypothesis that Dahl salt-sensitive (Dahl-S) rats exhibit distinct and separable phases of salt sensitivity.

Methods: Blood pressure (BP) telemetry was used to describe the detailed time course of salt-induced hypertension in Dahl-S rats and in hybrid rats derived from Dahl-S and Dahl salt-resistant strains.

Results: Switching to a high salt (4% NaCl) diet led to a biphasic increase in BP.

Characteristics of 24 h telemetered blood pressure in eNOS-knockout and C57Bl/6J control mice.

The purpose of the present study was to characterize in detail the 24 h blood pressure (BP) phenotype of mice lacking the gene for endothelial nitric oxide synthase (eNOS-/-) and the corresponding control strain (C57Bl/6J). Twenty-four hour BP recordings were made in conscious 12- to 16-week-old male mice 10 days following the implantation of a BP telemeter (n = 9 per group). The BP and heart rate of both strains were markedly affected by brief locomotor activity cycles, resulting in bimodal distributions of BP and heart rate within both light and dark periods.

Calcitropic gene expression suggests a role for the intraplacental yolk sac in maternal-fetal calcium exchange.

The expression of calcitropic genes and proteins was localized within murine placenta during late gestation (the time frame of active calcium transfer) with an analysis of several gene-deletion mouse models by immunohistochemistry and in situ hybridization. Parathyroid hormone-related protein (PTHrP), the PTH/PTHrP receptor, calcium receptor, calbindin-D(9k), Ca(2+)-ATPase, and vitamin D receptor were all highly expressed in a localized structure of the murine placenta, the intraplacental yolk sac, compared with trophoblasts. In the PTHrP gene-deleted or Pthrp-null placenta in which placental calcium transfer is decreased, calbindin-D(9k) expression was downregulated in the intraplacental yolk sac but not in the trophoblasts.