The American journal of physiology
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We evaluated the effects of 1 alpha,25-dihydroxycholecalciferol (1,25(OH)2D3), 24R,25-dihydroxycholecalciferol (24,25(OH)2D3), and 25-hydroxycholecalciferol (25(OH)D3) on the release of parathyroid hormone (PTH). Bovine parathyroid tissues were incubated in vitro for 4 h in low-calcium (1.0 mM) medium. 1,25(OH)2D3 ((10(-9)-10(-12)M), 24,25(OH)2D3 (10(-6)-10(-8)M), and 25(OH)D3 (5 X 10(-7)-5 X 10(-9)M) inhibited PTH release. ⋯ Inhibition by high concentrations of metabolites was evident by 1 h of incubation; inhibition was progressive throughout incubation, and maximal suppression to 30-40% of control occurred during the fourth and final hour of incubation. 1,25(OH)2D3 (10(-11) M), a low concentration that did not inhibit secretion, transiently stimulated release. In conclusion, under conditions of low-calcium-stimulated PTH release, 1,25(OH)2D3, 24,25(OH)2D3, and 25(OH)D3 inhibited PTH release, 1,25(OH)2D3 was the most potent inhibitor.
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Changes in cardiac output (Qco), heart rate, right atrial pressure, (Pra), and mean systemic pressure (Pms) in response to blood volume changes were measured in chronically prepared fetal sheep. With a 10% decrease in blood volume, fetal cardiac output, measured with the microsphere technique, decreased significantly from 592 +/- 28 to 471 +/- 32 ml . min-1 . kg-1. Heart rate changed little from control animals (163 +/- 5) to those with decreased volume (161 +/- 10 beats/min). ⋯ Heart rate again changed little (153 +/- 9 beats/min). The fact that cardiac output rose only a small amount, whereas right atrial pressure rose sharply with an increased blood volume, suggests that the fetal heart is operating near the upper limit of its Starling function curve. As a result, there is very limited cardiac reserve for increases in fetal cardiac output.
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Dopamine-beta-hydroxylase (DBH) and norepinephrine (NE) levels in superior mesenteric venous (SMV) and arterial blood and in intestinal lymph were determined sequentially before and during carotid artery occlusion (CAO) in anesthetized rabbits. During the first 15 min of CAO, SMV plasma NE increased 77% but SMV plasma DBH increased only 11%. During the second 15 min of CAO, SMV NE declined to 36% above control but SMV DBH rose further and peaked to 29% above control after CAO was released; arterial DBH and NE showed small insignificant changes. ⋯ In additional experiments, hepatic vein plasma NE was 74% lower than portal vein NE. Thus, during acute sympathetic activation, DBH and NE increase in mesenteric venous plasma and intestinal lymph but the peak response of plasma DBH lags behind that of NE. The degree of NE change in the general circulation is minimized due to hepatic clearance of NE.
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General features of the processes that contribute to renal potassium excretion are understood from clearance, stop-flow, micropuncture, and in vitro microperfusion experiments. However, the complex architecture of the kidney has made it difficult to examine individual nephron segments in all parts of the kidney. Accordingly, the extent to which distinguishable nephron populations, such as superficial and deep, may differ in their contributions to overall potassium excretion are not known. ⋯ Systemic factors that affect potassium excretion (potassium intake, sodium chloride intake, mineralocorticoid hormone levels, acid-base balance, and diuretic treatments) do so by modifying the net uptake of potassium from blood to cell and by altering the rate of fluid flow through the distal nephron. Under most circumstances, the distal nephron in the cortex appears to secrete potassium and the medullary collecting duct reabsorbs potassium. Although it is clear that successive nephron segments transport potassium in different ways, evidence to date does not indicate that potassium is handled differently by superficial nephrons compared to nephrons whose glomeruli lie in the deeper levels of the cortex.
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The heart rate response to hemorrhage was studied in conscious dogs before and up to 2 mo after the establishment of volume overload due to systemic arteriovenous (a-v) fistulas. Before a-v fistula, heart rate increased markedly during hemorrhage. When hemorrhage was preceded by dextran infusion, bleeding resulted in a gradual reduction in heart rate. ⋯ The response was observed as early as 5 days after a-v fistula. We conclude that an alteration in the heart rate response to hemorrhage appears early during volume overload. This alteration appears to be reflex in nature and to be mediated by the parasympathetic nervous system.