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Biomedical subjects

L Share

Publications and source records attributed to L Share.

At least 127 records · Page 7Linked to original sources
PubMed1980

Removal of immunoreactive arginine vasopressin by the perfused rat liver.

To assess the ability of the liver to remove immunoreactive arginine vasopressin (AVP) from the circulation and to determine the effect of certain metabolic factors on the process, a study was carried out with rat livers perfused at 37 C with an oxygenated albumin--electrolyte solution containing AVP (117 +/- 4.5 muU/ml). In controls, the hepatic clearance of AVP was 795 +/- 120 microliter/min (SEM). The addition of AVP in concentrations up to 9029 microU/ml, perfusion with a glucose-free medium, or perfusion without oxygen did not significantly alter the hepatic clearance of AVP. However, perfusion with cold medium (11 C) significantly altered AVP removal in that initially AVP removal increased, while later on AVP removal became completely inhibited. This phenomenon may possibly be a consequence of a cold-induced increase in hepatic AVP trapping which is rapidly saturated due to a cold-induced depression of AVP transport and degradation. Support for this thesis was provided by finding that high AVP concentrations depressed the cold-endhancing removal phase.

Animals↗
PubMed1980

Failure of acute intravascular volume expansion to alter plasma vasopressin in the nonhuman primate, Macaca fascicularis.

Experiments were carried out in the anesthetized monkey to determine the influence of acute hypervolemia on plasma vasopressin (ADH) concentration. The administration of an isotonic-isooncotic high molecular weight dextran infusion in two steps, each in an amount equal to 15% of the estimated blood volume, produced substantial elevations of left ventricular end diastolic pressure (17.1 cm H2O); however, no consistent change in mean plasma ADH concentration or mean arterial pressure occurred. The results support the position that in the primate, arterial blood pressure rather than blood volume is the major modulator of ADH secretion when blood volume is increased isoosmotically.

Animals↗
PubMed1980

Is vasopressin in the circulation of the dog freely filterable?

Studies were carried out to determine whether endogenously secreted vasopressin in the circulation of the dog is freely filterable. Blood from anaesthetized dogs was pumped through a dialysis coil and ultrafiltration was achieved by increasing the outflor pressure from the coil. In some cses, the dogs were hydrated before the experiment. A specific, precise radioimmunoassay was used to measure the concentration of vasopressin in the ultrafiltrate and the simultaneously sampled plasma. The concentration of vasopressin in the ultrafiltrate was consistently lower than that in the plasma at concentrations ranging from 1.7 to 335 micronmicron./ml in the latter, and the extent of the binding was lower in the hydrated than in the non-hydrated dogs. At plasma levels of vasopressin of 2-20 micrommicron./ml, vasopressin binding averaged only about 12%, whereas it averaged 40% at plasma concentrations greater than 20 micronmicrom./ml. This binding was not an artifact caused by some limitation of the ultrafiltration system because vasopressin dissolved in a salt solution and subjected to ultrafiltration in the system was freely filterable.

Animals↗
PubMed1980

The effect of meclofenamate on renal blood flow in the unanesthetized dog: relation to renal prostaglandins and sodium balance.

We compared the effects of sodium meclofenamate (5 mg/kg i.v.), an inhibitor of prostaglandin synthesis, on renal function in six unanesthetized dogs maintained for 5 to 7 days before the experiment on 100 mEq/day of NaCl and after sodium depletion by furosemide administration and salt deprivation. Plasma renin activity (PRA) during sodium depletion (12.35 +/- 3.93 ng ml-1 hr-1) was higher than during sodium repletion (1.46 +/- 0.47 ng ml-1 hr-1; P less than .05). The administration of meclofenamate did not alter mean arterial pressure, renal blood flow, urine volume, excretion of sodium and potassium or PRA in the sodium replete dog. However, during sodium depletion meclofenamate reduced renal blood flow from 168 +/- 35 to 105 +/- 23 ml/min (P less than .01) and urine flow from 0.32 +/- 0.09 to 0.16 +/- 0.05 ml/min (P less than .05) but did not affect mean arterial pressure, electrolyte excretion or PRA. The meclofenamate-induced reduction in renal blood flow during sodium depletion was well correlated with control PRA. After administration of meclofenamate, the urinary excretion of immunoreactive prostaglandin E2 fell by 66% (P less than .05) in the sodium replete dog and by 72% (P less than .05) in the sodium depleted dog. This study demonstrates that the effects of meclofenamate on renal hemodynamics vary with the state of sodium balance and in relation to PRA.

Anesthesia↗
PubMed1980

Antidiuresis and inhibition of PGE2 excretion by hyperoxia in the conscious dog.

Experiments were performed to determine the influence of varying inspired oxygen tension on renal prostaglandin E2 (PGE2) excretion, renal hemodynamics, and water and electrolyte excretion in the conscious dog. Hypoxic exposure (PIO2 = 56 torr) resulted in a 13% increase in renal blood flow (RBF), while hyperoxic breathing with PIO2 of 700, 1426, or 2139 torr, all resulted in significant 5--7% decline in RBF, a response that was significantly attenuated compared to the striking renal vasoconstriction caused by hyperoxia in anesthetized dogs. Hyperbaric oxygenation (HBO) (1426 torr O2, 2139 torr O2) was associated with unexpected decreases in urine flow (V) of 61% and 70%, respectively. The antidiuresis and mild hemodynamic adjustments were correlated with a 67% decline in urinary PGE2 excretion (UPGE2 x V) when the dogs breathed 700 torr O2, while exposure to 1426 torr O2 and 2139 torr O2 diminished UPGE2 x V by 92% and 99%, respectively. Plasma antidiuretic hormone (ADH) concentration, measured during exposure to 1426 torr O2, was unchanged. In addition, this nonpharmacologic hyperbaric decline in PGE2 excretion was not associated with any changes in sodium excretion of renin secretion, in contrast to the usual depression of these variables with pharmacologic PG inhibition (indomethacin). The HBO antidiuresis may be a consequence of an increased medullary osmotic gradient secondary to reduced vasa recta blood flow. Alternatively, this antiduresis could occur as a consequence of a lowering of the normal functional antagonism existing between PGE2 and ADH, such that the influence of endogenous ADH is potentiated.

Animals↗
PubMed1979

Renal effects of left atrial distension in dogs with chronic congestive heart failure.

The renal response to left atrial balloon inflation in normal dogs was compared with that in dogs with chronic congestive heart failure (CHF). CHF was induced by the production of an aortocaval fistula below the level of the renal arteries. CHF dogs showed elevated left ventricular end-diastolic pressure, enlarged hearts, a depression of myocardial contractility, pulmonary edema, ascites, and peripheral edema. They also showed significant decreases in urine flow, creatinine clearance, para-aminohippurate clearance, sodium and potassium excretion, fractional sodium excretion, osmolar clearance, arterial blood pressure, and heart rate. Balloon distension of the left atrium evoked a significant increase in urine flow and free-water clearance in the normal group. The reflex nature of this response was indicated by its blockade after bilateral cervical vagotomy. In contrast, the CHF group did not exhibit significant changes in urine flow or free-water clearance during balloon inflation. Plasma antidiuretic hormone (ADH) was significantly elevated in the CHF group; however, balloon distension reduced plasma ADH in both groups of dogs. Plasma renin activity was significantly elevated in the CHF dogs and was not changed by balloon distension in either group of dogs. It is concluded that animals with high-output CHF do not exhibit the atrial-diuretic reflex in spite of their ability to reduce ADH levels by atrial distension.

Animals↗
PubMed1979

The handling of immunoreactive vasopressin by the isolated perfused rat kidney.

Using the isolated rat kidney perfused with an artificial medium containing glucose as the sole fuel, we studied the renal handling of immunoreactive arginine vasopressin (AVP) and determined the effect of various factors on the ability of the kidney to remove AVP. In control kidneys perfused with AVP at concentrations below 116 muU/ml, the organ clearance of AVP (OC(AVP)) was 1,145+/-47 (SE) mul/min, whereas glomerular filtration rate (GFR) averaged 515+/-37 mul/min. Filtration could thus account for up to 45% of the OC(AVP), the balance presumably being cleared from the peritubular circulation. Of the AVP filtered, only 38% could be recovered in the urine (urinary clearance AVP averaged 205+/-12 mul/min) suggesting that the balance was taken up by the tubular epithelium and degraded. Fractional excretion of filtered AVP rose significantly in the presence of anoxia and cold (10 degrees C) to 49 and 59%, respectively, but was not affected by ouabain or high levels of AVP (458+/-58 muU/ml). The OC(AVP) was not significantly altered by the absence of glucose in the perfusate, anoxia, or ureteral ligation, maneuvers that were associated with significant reductions in GFR. In these and the control experiments, there was a significant inverse correlation between GFR and peritubular clearance emphasizing the importance of the latter (r = -0.749; P < 0.001). Cold, ouabain, and high concentrations of AVP reduced the clearance of AVP by the kidneys. On the basis of these studies we conclude that the kidney clears AVP from the circulation via two pathways, glomerular clearance and peritubular clearance. This exposes both the luminal and contraluminal surfaces of the tubular cells to the hormone, allowing these cells to remove AVP from the filtrate and the peritubular compartment. Noteworthy is the observation that under several conditions when GFR falls reducing the glomerular clearance of AVP, peritubular clearance increases and the total clearance of AVP by the kidney remains constant.

Albumins↗
PubMed1979

Interrelations between vasopressin and the renin-angiotensin system.

The interrelationships between vasopressin and the renin-angiotensin system are reviewed. Vasopressin can inhibit the release of renin by the kidney. This effect can occur at physiological plasma concentrations of vasopressin. Centrally administered angiotensin II can stimulate the release of vasopressin, a response that may be partially mediated by brain prostaglandins. The significance of this action of angiotensin II depends on whether there is an effective brain renin-angiotensin system and on whether peripherally generated or administered angiotensin can reach sites in the brain where it can act on vasopressin release. Peripherally administered angiotensin II can under certain, but not all, conditions stimulate vasopressin release. Peripheral angiotensin II can also potentiate the vasopressin response to an osmotic stimulus and to dehydration, but has little effect the release of vasopressin and renin, there is a failure to demonstrate any correlation between the two. Blockade of the renin-angiotensin system fails to modify the vasopressin response to a reduction in blood volume. In conclusion, the physiological significance of the interactions between the vasopressin and the renin-angiotensin system is not as yet clearly established.

Angiotensin II↗
PubMed1978

Vasopressin in the rat with spontaneous hypertension.

Because vasopressin is one of the most potent naturally occurring pressor agents, and because of its importance in the regulation of blood volume and composition, we have undertaken a study of the role of vasopressin in the pathogenesis of the hypertension in the Okamoto-Aoki spontaneously hypertension (SH) rat. In SH rats, systolic blood pressure increased from 135 +/- 3 (SE) mmHg at age 33 days to 184 +/- 3 mmHg at age 75 days (P less than 0.01). In the Wistar-Kyoto (WKY) control rats, blood pressure increased from 100 +/- 2 to 120 +/- 2 mmHg (P less than 0.01). The differences in blood pressure between the SH and WKY rats at all ages were significant (P less than 0.01). During the age period 33-75 days, the 24-h urinary excretion of vasopressin in the SH rat was consistently more than twofold greater (P less than 0.01) than in the WKY rat. Plasma vasopressin concentration and pituitary vasopressin content were also elevated in the SH rat (P less than 0.01 and P less than 0.02, respectively). Changes in systolic blood pressure in the SH rat, however, were not paralleled by changes in the urinary excretion of vasopressin. The data indicate that the secretion of vasopressin is elevated in the SH rat. However, the magnitude of this elevation, in and of itself, may not be sufficient to account for the rising blood pressure in the young SH rat.

Animals↗
PubMed1978

Effect of ventriculo-cisternal perfusion with angiotensin II and indomethacin on the plasma vasopressin concentration.

In anesthetized dogs, perfusion of the cerebral ventricles with indomethacin (IM), an inhibitor of prostaglandin biosynthesis, at rates of 1.9 or 7.6 microgram/min was without effect on the plasma ADH concentration. Ventriculo-cisternal perfusion with angiotensin II (AII; 19 ng/min) resulted in a 3-fold increase in the plasma ADH concentration within 45 min. When AII and IM were perfused together, the plasma ADH concentration increased only 2-fold, a response which was significantly lower than that obtained with AII alone. Thus, the ability of central AII to stimulate ADH release may depend, at least in part, upon the local release of prostaglandins.

Angiotensin II↗
PubMed1976

Metabolic clearance of immunoreactive vasopressin and immunoreactive [131I]iodo vasopressin in the hypophysectomized dog.

Fourteen acutely hypophysectomized, anesthetized dogs were given a constant infusion of arginine vasopressin (AVP) and 131I-labeled arginine vasopressin ([131I]AVP). After 90 min, 3 blood samples were collected at 15 min intervals for determination of total body clearances of immunoreactive AVP and immunoreactive [131I]AVP. Seven dogs were then nephrectomized. Ninety minutes later, a second set of 3 blood samples was collected at 15 min intervals for clearance measurements in these and the 7 time-control dogs. Prenephrectomy AVP clearance averaged 5.1+/-1.0 ml/min-kg (mean +/- SE, n=7), and the 210-240 min postnephrectomy AVP clearance average 4.9+/-0.8. The 90-120 min average clearance in the time-control dogs was 6.1+/-0.9 ml/min-kg (n=7) and AVP clearance in these dogs increased (P less than 0.01) with time to 7.3+/-0.9 ml/min-kg during the 210-240 min period of constant infusion. Although the postnephrectomy AVP clearance was not significantly changed from prenephrectomy levels, it was significantly lower (P less than 0.05) than the 210-240 min average clearance in the time-controls. Clearance of [131I]AVP was 3.3+/-0.2 ml/min-kg (n=7) before nephrectomy and 2.9+/-0.2 ml/min-kg after nephrectomy. This was a significant 12% reduction (P less than 0.01). [131I]AVP clearance in the time control dogs was 3.9+/-0.3 during 90-120 min of infusion and 3.9+/-0.4 during 210-240 min of infusion. [131I]AVP clearance before nephrectomy was 79+/-12% of AVP clearance (P less than 0.005) and afther nephrectomy was 74+/-16% of AVP clearance (P less than 0.05). Although these results might suggest that [131I]AVP clearance is at least a qualitative indicator of AVP clearance, there was no significant correlation (P less than 0.20) between AVP clearance and [131I]AVP clearance.

Animals↗
PubMed1976

Vasopressin release during ventriculo-cisternal perfusion with prostaglandin E2 in the dog.

In an attempt to determine whether prostaglandin E2 (PGE2) can act centrally to affect the release of vasopressin (ADH), the ventriculo-cisternal system of anaesthetized dogs was perfused with PGE2. When PGE2 was perfused at a rate of 76-4 ng/min (0-19 ml/min), the plasma ADH concentration was unchanged. However, perfusion of PGE2 at a rate of 152-8 ng/min (0-19 ml/min) resulted in a significant increase in the plasma ADH concentration from the control value of 9-0 +/- 2-2 (S.E.M.) to 18-8 +/- 3-9 muu./ml at 10 min and to 41-0 +/- 16-7 muu./ml at 30 min after the start of the perfusion. There were no changes in arterial blood pressure, rectal temperature, plasma osmolality, and the plasma concentrations of sodium and potassium. In additional experiments, i.v. injection of indomethacin (2 or 20 mg/kg) decreased the plasma ADH concentration by approximately 50%. Although this finding is consistent with a role of PGE2 in the control of ADH release, it could also have been due to the observed increases in arterial blood pressure and effective left atrial pressure. Plasma renin activity was unchanged in the indomethacin experiments. It is concluded that PGE2 can act in the central nervous system to stimulate ADH release.

Animals↗
PubMed1975

Treatment of patients with severe hypertension by inhibition of angiotensin-converting enzyme.

1. The results of the administration of the nona-peptide inhibitor (SQ 20,881) of the enzymatic conversion of angiotensin I into angiotensin II in twelve severe hypertensive patients are presented. 2. Administration of the compound was associated with a fall in blood pressure in ten of twelve patients. 3. Four patients had a normal plasma renin activity (PRA) with a range of 1.6-3.7 ng h-1 ml-1 and eight patients had a high PRA with a range of 5.0-74 ng h-1 ml-1. Two of the patients with normal PRA had no fall in blood pressure despite receiving 2 mg/kg of the compound. Two patients with normal PRA, however, did respond, thus indicating that a high PRA is not necessary for a response to the inhibitor compound. 4. It was found that haemodialysis or diuresis with frusemide enhanced the blood pressure response to the compound. 5. The presence of a measured low total blood volume was found to be associated with an exaggerated fall in blood pressure to a small dose of compound (0.125 mg/kg) in one patient.

Blood Pressure↗
PubMed1975

Vasopressin release during nonhypotensive hemorrhage and angiotensin II infusion.

These experiments were designed to determine whether angiotensin II (AII) could potentiate the increase in plasma vasopressin (ADH) concentration produced by continuous, nonhypotensive hemorrhage in nephrectomized dogs. Infusion of AII (10 ng/kg.min) into a common carotid artery in nonbled dogs did not increase plasma ADH levels, suggesting that increases in carotid arterial plasma AII concentration alone do not stimulate an increase in ADH release. Subsequently, nephrectomized dogs subjected to nonhypotensive hemorrhage (0.44 ml/kg.min) were infused as follows: 0.9% saline intravenously, AII (10 ng/kg.min) intravenously, or AII (10 ng/kg.min) into the carotid. The Plasma ADH concentration increased in all three groups of dogs during hemorrhage. Although the AII-infused dogs demonstrated significant increases in plasma ADH levels earlier during hemorrhage, these changes were small; there were no statistically significant differences in plasma ADH concentrations among the three groups. These results suggest that increases in plasma AII concentration have little or no significant effect on the volume control of ADH release.

Angiotensin II↗
PubMed1975

Malignant hypertension due to musculo-mucoid intimal hyperplasia of intrarenal arteries. Absence of renal fibrinoid necrosis.

Severe essential hypertension in a subset of American black subjects is associated with marked stenosis of interlobular arteries and arterioles of the kidneys, observed by renal biopsy and binephrectomy specimens. The interlobular arterial stenosis is caused by marked thickening of the intima due mainly to the presence of smooth muscle cells, basement membrane material, and acid mucopolysaccharide. Because of this makeup, we propose the term "musculo-mucoid intimal hyperplasia" for this lesion. The media of these arteries appears maximally dilated, and by electron microscope displays degenerative changes of the smooth muscle cells. The arterioles are thickened, due mainly to hyalinization, but also due to the musculo-mucoid change (onionskin effect). The smooth muscle cells are degenerated and atrophic. These patients do not exhibit fibrinoid necrosis of the arteries, arterioles, and glomeruli, presumably because of the rapidity of the development of the arterial stenotic lesion. Accordingly, the glomeruli are destroyed by ischemia, and there is no evidence of glomerulitis (no "Kombinations" form of Fahr). A unifying hypothesis concerning renal hypertensive arterial disease is suggested by these studies. This hypothesis places the main emphasis for all the morphological expressions of the intrinsic visceral vasculature on changes involving the main functional unit of the vessel wall, the medical smooth muscle.

Acute Kidney Injury↗