Case report: persistent dysuria and a suprapubic mass in a 3-year-old boy.
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Child, Preschool↗
Biomedical subjects
Robert M Weiss
Publications and source records attributed to Robert M Weiss.
Forebrain-mediated adaptations to myocardial infarction in the rat.
Recent studies suggest that the forebrain contributes to the circulatory derangements leading to heart failure after myocardial injury. We tested that hypothesis by examining the effect of myocardial infarction (MI) or sham MI (MI-s) on neurohumoral regulation in rats with prior anteroventral (AV) third ventricle lesion (AV3V-x) or sham lesion (AV3V-s). AV3V-s/MI rats had higher sodium intake, lower urine volume, and lower urinary sodium excretion than AV3V-s/MI-s rats. AV3V-x/MI rats had lower sodium intake and higher urine volume than AV3V-s/MI or AV3V-s/MI-s rats and urinary sodium excretion comparable to AV3V-s/MI-s rats. AV3V-x had no effect on baseline plasma renin activity (PRA). One week after MI, PRA had increased in AV3V-s but decreased in AV3V-x rats. AV3V-x reduced renal sympathetic nerve activity in MI and MI-s rats. AV3V-x improved baroreflex function in MI rats but diminished it in MI-s rats. Survival beyond 2 wk was lower in the AV3V-x/MI rats than in all other groups. These results confirm a critical role for the forebrain in the neurohumoral adjustments to MI.
Adaptation, Physiological↗
The renin-angiotensin-aldosterone system excites hypothalamic paraventricular nucleus neurons in heart failure.
The paraventricular nucleus (PVN) of the hypothalamus has critical homeostatic functions, including the regulation of fluid balance and sympathetic drive. It has been suggested that altered activity of this nucleus contributes to the progression of congestive heart failure (HF). We hypothesized that forebrain influences of the renin-angiotensin-aldosterone system augment the activity of PVN neurons in HF. The rate of PVN neurons (n = 68) from rats with ischemia-induced HF was higher than that of PVN neurons (n = 42) from sham-operated controls (8.7 +/- 0.8 vs. 2.7 +/- 0.3 spikes/s, P < 0.001, HF vs. SHAM). Forebrain-directed intracarotid artery injections of the angiotensin type 1 receptor antagonist losartan, the angiotensin-converting enzyme inhibitor captopril, and the mineralocorticoid receptor antagonist spironolactone all significantly (P < 0.05) reduced PVN neuronal activity in HF rats. These findings demonstrate that the renin-angiotensin-aldosterone system drives PVN neuronal activity in HF, likely resulting in increased sympathetic drive and volume accumulation. This mechanism of neurohumoral excitation in HF is accessible to manipulation by blood-borne therapeutic agents.
Action Potentials↗
Discovery of a spontaneous genetic mouse model of preeclampsia.
Preeclampsia remains a leading cause of maternal and fetal morbidity and mortality but has an unknown etiology. Women with elevated baseline blood pressure have an increased risk of this disorder. We hypothesized that BPH/5 mice, an inbred mouse strain with mildly elevated blood pressure, would develop a pregnancy-induced hypertensive syndrome. Nonpregnant female BPH/5 and C57BL/6 mice underwent thoracic aortic implantation of telemeters. After 7 days of recovery and 5 days of baseline mean arterial blood pressure (MAP) recording, strain-matched timed matings were carried out. MAP was recorded continuously during pregnancy and for 1 week after birth. In separate mice in metabolic cages, urinary protein was tracked, followed by renal histological analysis. Before pregnancy, the BPH/5 strain had elevated baseline MAP compared with the C57BL/6 strain, but both strains had similar total urinary protein levels and renal histology. MAP remained stable in both groups during the first 2 weeks of pregnancy. However, at the start of the last trimester, MAP began to rise further in the BPH/5 mice; it rose to peak levels just before delivery and returned to prepregnancy levels by 2 days after delivery. This was accompanied by late-gestational proteinuria and progressive glomerulosclerosis. No changes were observed in the C57BL/6 group except for a small decrease in MAP at mid gestation. The BPH/5 group delivered significantly smaller litters despite normal numbers of fetuses early in gestation, and longitudinal ultrasound studies documented fetal demise before the onset of hypertension and renal disease. This is the first report of an animal model that spontaneously develops a syndrome that bears close resemblance to preeclampsia, and it should have an impact on our understanding of the pathophysiology of this disorder.
Animals↗
Quantification of endothelins, their receptors, and endothelin-converting enzyme mRNAs in rat genitourinary tract using real-time RT-PCR.
INTRODUCTION: Quantification of mRNA expression is essential for the assessment of endothelin (ET) receptor-mediated mechanisms. Recently, a novel technique for the determination of mRNA expression, termed real-time reverse transcription polymerase chain reaction (RT-PCR), has been developed. We therefore applied real-time PCR using SYBR Green I to quantify ET-1, ET-3, ET-converting enzyme-1 (ECE-1), and ETA and ETB receptor subtype mRNA expression in the rat genitourinary tract. METHODS: The cDNA was synthesized by RT of RNA extracted from the rat bladder, ventral prostate, dorsolateral prostate, and vas deferens. All steps subsequent to the RT reaction were carried out by the thermal cycler/detector and computer-assisted programs processed a quantitative result. RESULTS: Designing optimal primer sequences that minimized primer-dimer formation and adjusting annealing temperatures that prevented nonspecific product amplification have made it possible to identify a single peak in the melt curve and to obtain an appropriate standard curve for each gene transcript. In our experiments, input cDNA levels as low as 100 copies of the product could be detected. DISCUSSION: We demonstrated that significant quantitative variations existed in the expression levels of ET-1, ET-3, ECE-1, and ETA and ETB receptor subtype mRNAs within a tissue and between different regions of the genitourinary tract and that the predominant expression of ETs and their receptor mRNAs in all tissues studied were ET-1 and the ETA receptor subtype, respectively.
Animals↗