The American journal of physiology
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The purpose of this review is to illustrate the application of molecular methodologies to the investigation of a fundamentally integrative problem in renal physiology, namely, the mechanism of regulation of water excretion by the kidney and the concomitant concentration of solutes in the urine. A new revolution in renal physiology is occurring as new research tools have become available as a result of the cloning of cDNAs for many of the major transporters and receptors in the renal medulla. ⋯ In addition, two collecting duct water channels, aquaporin-2 and aquaporin-3, are targets for long-term regulation by vasopressin through effects on the absolute expression levels of the water channel proteins. This review focuses on the mechanisms of both short- and long-term regulation of these water channels by vasopressin.
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Net transfer of blood volume into or out of the cardiac chambers should have the same effect on central venous pressure as does transfer of an equal volume of blood to or from peripheral organs (e.g., spleen, or liver). We studied five pentobarbital sodium-anesthetized open-chest pigs (20-23 kg) to determine whether a reduction in the time-averaged volume of blood contained in the heart, induced by rapid atrial pacing, can raise right atrial pressure. A central premise of our study is that the mean value of right atrial pressure is acutely governed by the volume of blood that distends the central veins, and that atrial contractions primarily determine how atrial pressure varies about its mean value. ⋯ Mean right atrial pressure rose abruptly from 2.8 +/- 0.5 mmHg during normal sinus rhythm to 3.5 +/- 0.5 mmHg (P = 0.015) at the onset of rapid pacing in these four pigs, presumably owing to decreased cardiac blood volume and a reciprocal expansion of central venous volume. In the fifth pig, a reduction in cardiac output induced by tachycardia led to a larger rise in mean right atrial pressure than did a reduction in cardiac output induced by bradycardia, presumably because tachycardia reduces cardiac blood volume whereas bradycardia raises cardiac volume. We conclude that the heart may play an important role in maintaining or raising its own filling pressure when heart rate rises.
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Two series of experiments were done in male Wistar rats to investigate the medullary pathways that mediate the depressor responses from sodium-sensitive sites in the nucleus of the solitary tract (NTS). In the first series, the anterograde tract tracer Phaseolus vulgaris leucoagglutinin (PHA-L) was iontophoresed unilaterally at sites in the NTS at which microinjections (20 nl) of a 154-175 mM NaCl solution elicited depressor responses. PHA-L injection sites were found to be localized within the medial subnucleus of the NTS (Sm). ⋯ In the second series of experiments, the effect of blocking synaptic transmission in VLM with cobalt chloride (CoCl2; 5 mM, 100 nl) on the cardiovascular response elicited by microinjection (20 nl) of hypertonic saline (154-175 mM) into the ipsilateral Sm was investigated in the alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rat. Microinjection of CoCl2 into VLM, at sites shown in the previous study to receive efferent projections from Sm, significantly attenuated the depressor (60%) and bradycardic (80%) responses to stimulation of Sm. These data indicate that the sodium-sensitive region of the caudal Sm innervates VLM neurons and suggest that these VLM neurons are involved in mediating the depressor and bradycardic responses elicited by changes in the extracellular concentration of sodium.