Hypertensive disorders of pregnancy continue to be a significant source of maternal and fetal morbidity and mortality, and recent evidence suggests that the incidence of preeclampsia (PE) is increasing. Recent epidemiological studies indicate that the effects of PE may persist long after pregnancy, in both the mother and the offspring, as increased incidence of cardiovascular disease. The last decade has produced new insights into the pathogenesis of PE. The initiating event in PE appears to be impaired placental perfusion and subsequent placental ischemia, which results in the elaboration of numerous factors. Factors such as soluble fms-like tyrosine kinase-1, soluble endoglin and the angiotensin II type-1 receptor autoantibodies contribute to maternal endothelial and cardiovascular dysfunction, marked by increased reactive oxygen species and decreased bioavailable VEGF, nitric oxide and prostacyclin. However, the importance of the various endothelial and humoral factors that mediate these changes during PE remain to be elucidated. Keywords cardiac; cytokines; pregnancy; VEGF Clinical significance of the hypertensive disorders of pregnancyPreeclampsia (PE) is a pregnancy-specific syndrome characterized by new-onset hypertension and proteinuria manifesting after 20 weeks of gestation, which may progress and cause injury to the blood vessels of major organs, such as the liver and the brain. The hepatic and neuro logical complications of PE make it a potentially deadly disease, especially when tertiary obstetrical care is lacking. Consequently, PE remains a considerable obstetric problem and a significant source of maternal and neonatal morbidity and mortality [1].

We evaluated pressure-dependent stimulation of renin release in rats with sustained hypertension induced by chronic blockade of nitric oxide synthase with N omega-nitro-L-arginine methyl ester (L-NAME) for 5 to 7 days. Rats were anesthetized and catheters were inserted into the carotid artery and abdominal aorta for measurement of arterial pressures. An adjustable snare was placed around the suprarenal aorta, and this snare was tightened to reduce renal perfusion pressure. Pressure-dependent renin release was evaluated in hypertensive rats by reducing renal perfusion pressure to 125, 85, and 65 mm Hg. Renin release was also evaluated in normotensive control rats at these same pressures. Basal systemic arterial pressures averaged 159 +/- 3 and 124 +/- 4 mm Hg (P < .001), respectively, in the L-NAME-treated (n = 22) and normotensive control (n = 18) rats. Basal plasma renin activity was lower in L-NAME than control rats (5.0 +/- 0.3 versus 9.5 +/- 1.3 U, P < .01), and plasma renin activity was markedly attenuated at all comparable levels of renal perfusion pressure. Maximal plasma renin activity levels were achieved at perfusion pressures reduced to 65 mm Hg, and plasma renin activity averaged 14 +/- 2 and 34 +/- 7 U (P < .01) in L-NAME hypertensive and control rats, respectively. However, infusion of the nitric oxide donor sodium nitroprusside similarly stimulated plasma renin activity levels to 39 +/- 3 and 45 +/- 3 U (P > .05), in the hypertensive and normal control groups, respectively. Overall, these findings are consistent with the hypothesis that prolonged L-NAME administration attenuates pressure-dependent renin release by inhibiting nitric oxide formation, which may function as a paracrine mechanism inversely linking renal perfusion pressure with the stimulation of renin release.

Using sucrose-sweetened diet as a control, increased weight gain with the ingestion of NNS was observed. However, using a nonsweetened control, neither increased caloric intake nor weight gain occurred with NNS intake. Alternating diets between NNS, NS, and control did not affect the appetite.

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Prior work found an increase in renal sodium excretion in male spontaneously hypertensive rats (SHR) following dorsal spinal column stimulation (DCS) at the spinal segment of the left renal sensory nerves (T12–T13). General sympathetic tone, and renal blood flow were unaltered by DCS. The effects of dorsal rhizotomy on the DCS‐induced renal sodium excretion was investigated in male SHR. SHR were randomly assigned to one of the following groups: no‐stimulation (NS), stimulation (S), no stimulation + Rhizotomy (NS+R), and Stimulation + Rhizotomy (S+R). Stimulated rats received DCS during the 2nd of five 15‐min. collection periods. Blood pressure was measured via a carotid artery cannula, and urine was collected via a bladder cannula. A standard stimulation parameter of 66% of the motor threshold (0.2 msec duration and 50 Hz) was used. Urine sodium was analyzed using flame photometry. Sodium excretion was significantly elevated in periods 3 and 4 in the S group when compared with corresponding periods in the NS group. Sodium excretion was significantly elevated in period 5 in the S+R group when compared with the NS+R. There were no differences between the S+R and the S groups. The DSC‐induced increase in sodium excretion is independent of retrograde signaling in the renal nerves. This research was funded by a departmental grant, in the Department of the Biological Sciences, Minnesota State University, Mankato, MN