Biomedical subjects

R L Zerbe

Publications and source records attributed to R L Zerbe.

50 records · Page 3Linked to original sources

PubMed1982

Mechanisms involved in central cardiovascular effects of prostaglandin F2 alpha.

Prostaglandin F2 alpha (PGF2 alpha) injected into the cerebroventricular system (icv) of halothane-anesthetized rats increased the arterial blood pressure, heart rate, and rectal temperature. These effects were accompanied by a preferential increase in plasma norepinephrine concentration. Plasma levels of epinephrine, renin, and vasopressin were not changed in the PGF2 alpha-icv-treated rats. Bilateral vagotomy did not affect the PGF2 alpha-induced hypertension and tachycardia nor was there any change in the selective increase in plasma norepinephrine concentration. Hexamethonium pretreatment suppressed, in a dose-response manner, the increases in blood pressure, heart rate, and rectal temperature in response to PGF2 alpha-icv. Plasma norepinephrine and epinephrine levels were not altered by PGF2 alpha-icv in hexamethonium-treated rats, but plasma vasopressin concentration was markedly elevated in all hexamethonium-infused rats. These results suggest that selective central activation of the sympathetic nervous system underlies the profound cardiovascular and temperature responses elicited by central administration of PGF2 alpha.

Animals↗

PubMed1982

Cardiovascular, sympathetic, and renin-angiotensin system responses to hemorrhage in vasopressin-deficient rats.

To determine if the subnormal blood pressure recovery after hemorrhage in Brattleboro rats is due to secondary abnormalities in the renin-angiotensin or sympathetic nervous systems, we measured the hemodynamic, catecholamine, and renin activity responses to moderate acute hemorrhage in anesthetized Brattleboro rats. Results were compared to responses in groups of animals matched for either age or weight. Blood pressure recovery was significantly blunted (P less than 0.01) in Brattleboro rats compared to that in either control group, but heart rate responses were similar. Basal plasma norepinephrine was significantly higher in Brattleboro rats than in controls (P less than 0.001), but the response to hemorrhage was not significantly different. Both plasma epinephrine levels and renin activity were significantly higher before hemorrhage and increased more after hemorrhage in vasopressin-deficient animals. Plasma vasopressin in controls increased approximately 10-fold, reaching levels of 790 +/- 140 pg/ml in age-matched controls and 425 +/- 60 pg/ml in weight-matched controls. Vasopressin levels in Brattleboro rats were undetectable both before and after hemorrhage. We conclude from these data that the subnormal blood pressure recovery observed in vasopressin-deficient rats is not due to secondary abnormalities of the renin-angiotensin or sympathetic nervous systems, but, instead, is related more directly to the vasopressin deficiency.

Animals↗

PubMed1981

A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria.

The diagnoses provided by a standard indirect test of vasopressin function were compared with those obtained by radioimmunoassay of plasma vasopressin in 24 patients with nonglucosuric polyuria. All seven cases of severe neurogenic diabetes insipidus diagnosed by the indirect tests were confirmed by the vasopressin assay. However, two of six patients with partial neurogenic diabetes insipidus by indirect criteria had normal vasopressin secretion by the direct assay; one was found to have primary polydipsia, and the other nephrogenic diabetes insipidus. Moreover, three of 10 patients diagnosed as having primary polydipsia by the indirect test had clear evidence of partial vasopressin deficiency by the direct assay. The inability of the indirect test to distinguish accurately between partial neurogenic diabetes insipidus and primary polydipsia may be explained by increased sensitivity to low concentrations of vasopressin in the former disorder and a reduction of maximal concentrating ability in both. We conclude that the incorporation of a vasopressin assay improves accuracy in the differential diagnosis of polyuria.

Adolescent↗

PubMed1981

Effect of captopril on cardiovascular, sympathetic and vasopressin responses to hemorrhage.

Spontaneous blood pressure recovery following hemorrhage in anesthetized rats is almost completely blocked by administration of captopril. This occurs despite comparable or enhanced increases in plasma levels of catecholamines and vasopressin. These findings suggest that angiotensin II, the formation of which is blocked by captopril, is essential to acute blood pressure recovery following hemorrhage and that changes in catecholamines or vasopressin are insufficient to sustain pressure recovery. The data also indicate that angiotensin II formation is not essential in the hemorrhagic stimulation of vasopressin or catecholamines.

Animals↗

PubMed1981

Catecholamines and vasopressin in forebrain nuclei of hypertension prone and resistant rats.

Catecholamine and vasopressin content were studied in discrete brain nuclei of the Sabra strain of hypertension prone (SBH) and resistant (SBN) rats. Higher concentrations of dopamine, norepinephrine and epinephrine were observed in the median eminence of SBN compared to SBH or controls (SB) rats. Dopamine and epinephrine levels were higher in the lateral septal nucleus of SBH rats as compared to SBN or SB. Vasopressin content in discrete regions along the hypothalamo-pituitary axis was elevated in both SBH and SBN as compared to SB, but were especially elevated in the SBH group. The catecholamine and vasopressin changes found in SBH are different than those described in other genetically hypertensive rats indicating a difference in either the pathogenesis or central response to hypertension of this strain.

Animals↗

PubMed1981

Arginine vasopressin response to insulin-induced hypoglycemia in man.

Insulin-induced hypoglycemia causes an increase in plasma vasopressin concentration in man and rat. To assess the mechanism by which this occurs, the effect of hypoglycemia was studied in healthy adults. After insulin injection, a 7-fold rise in plasma immunoreactive arginine vasopressin to 8.2 +/- 3.6 pg/ml was observed in 10 normal subjects. This was associated with a rise in plasma sodium of 2 meq/liter, but no significant change in mean arterial pressure or hematocrit was observed. The significance of the plasma sodium rise was assessed by observing the vasopressin response to hypoglycemia in a patient shown previously to have a selective loss of the vasopressin response to osmotic stimulation. His plasma vasopressin rose from 1.6 to 12.5 pg/ml with no fall in blood pressure or volume. beta-Adrenergic blockade with propranolol before repeat insulin-induced hypoglycemia did not reduce the vasopressin response (peak plasma vasopressin, 8.1 +/- 1.7 pg/ml), despite suppression of PRA. Linear regression analysis showed that the rise in plasma vasopressin and the percentage decline in plasma glucose correlated significantly (r = 0.57, P less than 0.001). In conclusion, hypoglycemia releases vasopressin nonosmotically by a mechanism that appears to be independent of factors currently known to effect vasopressin secretion.

Adult↗

PubMed1979

Plasma vasopressin in uncontrolled diabetes mellitus.

Concentrations of the antidiuretic hormone, arginine vasopressin, were measured in 28 patients with severe hyperglycemia to determine if abnormalities in hormonal regulation of water excretion could contribute to the extreme dehydration of uncontrolled diabetes mellitus. Vasopressin levels were markedly elevated in both nonketotic and ketotic patients, indicating that vasopressin deficiency plays no role in the polyuria that accompanies hyperglycemia. Instead, the observed increases in vasopressin represent an ineffective effort to conserve water in the face of an overwhelming solute diuresis caused by the glucosuria. The reasons for such marked elevations in plasma vasopressin in these diabetic patients are multifactorial. Both groups of diabetic patients had evidence of hypovolemia, which was sufficient in magnitude to stimulate vasopressin release. Furthermore, nausea provided an independent stimulus to vasopressin secretion in many patients. Osmotic stimulation might have resulted from the large fraction of unidentified plasma solutes, but this factor alone was not sufficient to explain the markedly increased concentrations of vasopressin. Whether such elevations in vasopressin could have metabolic and/or hemodynamic effects in uncrontrolled diabetes remains to be established.

Adolescent↗

PubMedDate not supplied

The prognosis of hyponatremia at hospital admission.

To assess the risk of mortality in patients with hyponatremia at the time of hospital admission, the authors studied data for 13,979 patients admitted over a 46-month period. Of the 763 (4%) admitted with hyponatremia, 757 (99%) were matched by age, gender, and admitting date with normonatremic control patients. Hyponatremic patients were more than seven times as likely to die in the hospital than the control patients, and they were more than twice as likely to die after discharge (p less than 0.0001 for both). This relationship with in- and outpatient mortality held when controlling for the diagnoses found more often in the hyponatremic patients. Hyponatremia appears to be an indicator of increased risk of death regardless of the disease with which it is associated.

Adult↗

PubMedDate not supplied

A new Met-enkephalin analogue suppresses plasma vasopressin in man.

Metkephamid acetate, a newly synthetized analogue of methionine enkephalin, suppressed plasma vasopressin levels from 2.4 pg/ml to 0.8 pg/ml after intramuscular administration to 4 normal human volunteers. This suppression occurred in the absence of significant changes in either plasma osmolality or blood pressure. Thus, metkephamid acetate, like many other opiates which bind to the mu subtype of opiate receptors, has a direct suppressive effect on plasma vasopressin levels.

Blood Glucose↗

PubMedDate not supplied

Vasopressin: an essential pressor factor for blood pressure recovery following hemorrhage.

Two experimental approaches were used to evaluate the importance of the pressor effects of vasopressin in blood pressure recovery following hypotensive hemorrhage. Experiments using homozygous Brattleboro rats demonstrated that the hemodynamic recovery of these animals was subnormal, even though the activation and efficacy of the sympathetic nervous and renin-angiotensin systems were intact. Experiments using an antipressor vasopressin analogue in normal rats during hypotensive hemorrhage demonstrated significantly blunted blood pressure recovery in the presence of the analogue. Thus, both experiments indicate that the pressor effects of circulating vasopressin play an essential role in blood pressure recovery following hypovolemic hypotension induced by hemorrhage.

Angiotensin II↗

PubMedDate not supplied

Central cardiovascular effects of mammalian neurohypophyseal peptides in conscious rats.

To confirm and extend the results of previous studies which demonstrated central cardiovascular effects of vasopressin in anesthetized rats, we determined blood pressure and heart rate changes for 30 minutes after intracerebroventricular injections of arginine vasopressin, arginine vasotocin and oxytocin in conscious rats. As compared to sham injections, significantly greater increases in either systolic or diastolic blood pressure were noted over the 30 minutes which followed the injection of 0.15, 1.0 or 10.0 nM of either vasopressin or vasotocin. In animals given vasopressin, plasma levels of the peptide were determined. There was a substantial increase in plasma vasopressin only after the highest dose. Overall blood pressure responses to doses of oxytocin as high as 100 nM were not significantly different than sham injections. Heart rate following both vasopressin and vasotocin was increased at 0.15 nM, was initially decreased then increased at 1.0 nM and was substantially decreased after the 10.0 nM dose. There was a significant increase in heart rate at the 10.0 nM and 100 nM doses of oxytocin. Dose response curves for systolic blood pressure and heart rate 20 minutes after injection were similar for vasopressin and vasotocin. We conclude that arginine vasopressin has significant central pressor and tachycardic effects in conscious rats, and it is related, at least in part, to the tail structure of the peptide, which is shared with arginine vasotocin.

Animals↗

PubMedDate not supplied

Alteration of cardiovascular, neurogenic, and humoral responses to acute hypovolemic hypotension by administered prostacyclin.

Acute hypovolemia induced by bleeding (5 ml/300 g body weight) halothane-anesthetized (0.8% in oxygen) rats is attended by hypotension, bradycardia, and increases in plasma renin, vasopressin, and catecholamine levels. Infusion of prostacyclin (PGI2, O.03 microgram/kg.min) to acutely hemorrhaged rats enhanced recuperation of heart rate, and potentiated the sympathetic response and vasopressin release without altering blood pressure of plasma renin concentration (PRC). Bleeding of bilaterally adrenal demedullated, splanchnicectomized rats resulted in prolonged hypotension and increased plasma levels of vasopressin and renin; epinephrine in the plasma was not detectable, and plasma norepinephrine concentration was not increased after hemorrhage. Prostacyclin infusion to the demedullated, splanchnicectomized rats had no effect on heart rate but enhanced blood pressure recovery after hemorrhage; in this experimental group, PRC was markedly elevated but prostacyclin had no effect on plasma vasopressin or catecholamine concentrations. In rats exposed to severe bleeding, resulting in a nonreversible shock and high mortality, PGI2 infusion after the bleeding increased the survival rate without effect on blood pressure, heart rate, or circulating levels of vasopressin and catecholamines. This study suggests that prostacyclin, through stimulation of the sympathoadrenal axis, enhances heart rate recuperation and vasopressin release in response to acute hemorrhagic shock. Furthermore, prostacyclin may stimulate renin secretion in sufficient amount to compensate for the inadequate sympathetic response during hemorrhagic shock. It is also shown that prostacyclin improves the survival rate to severe hemorrhage without overt hemodynamic or sympathetic effects.

Angiotensin II↗

PubMedDate not supplied

Opiate receptors and cardiovascular control in conscious SHR and WKY rats.

This study examined the cardiovascular, respiratory, and sympathetic effects of selective mu and delta opioid agonists microinjected into the hypothalamic nucleus preopticus medialis (POM) of conscious SHR and WKY rats. The mu receptor agonist D-Ala2-MePhe4-Gly5-ol-enkephalin (DAGO) at a dose of 0.6 or 6.0 nanomoles (Nmol) increased the blood pressure and heart rate in WKY rats. In SHR rats, the lower dose of DAGO similarly had a pressor effect whereas the higher dose was depressor; heart rat was increased only by the 6.0 nmol dose in these animals. In both SHR and WKY rats, this opioid caused respiratory acidosis and elevation of plasma norepinephrine (NE) and epinephrine (E); plasma vasopressin was reduced by the higher dose of DAGO. All of these effects of the mu agonist were reversed by the opiate receptor antagonist naloxone (0.5 mg/kg, i.a.). The delta opiate-receptor agonist D-Ala2-D-leu5-eukephalin at a dose of 6.0 or 20.0 nmol increased blood pressure and heart rate in both SHR and WKY rats without affecting respiratory variables. Plasma NE and EPI were elevated at the peak of the pressor period. These studies suggest that the anteroventral hypothalamic region may be an important site in central autonomic regulation by opioid peptides. The mu-receptor agonist was more potent than the delta agonist in eliciting cardiovascular and respiratory effects and associated sympatho-adrenomedullary activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Role of catecholamines and vasopressin in cardiovascular responses to bilateral dorsolateral transection of the medulla oblongata in the rat.

The role of sympathetic and other pressor systems in the development of fulminant hypertension induced by baroreceptor deafferentation is still unclear. We studied the effects of acute hypertension produced by bilateral dorsomedullary knife cuts lateral to the nucleus tractus solitarii (DMK-cut) on plasma norepinephrine (NE), epinephrine (E), and vasopressin (VP) in conscious, tail-artery-cannulated rats. In saline-pretreated (SAL) rats, DMK-cut caused a significant (p less than 0.001) rise in mean blood pressure (MAP, +68 +/- 3 mm Hg), heart rate (HR, +97 +/- 19 bpm), NE (+2.5 +/- 0.3 ng/ml), E (+2.7 +/- 0.4 ng/ml), and VP (+115 +/- 34 pg/ml) compared to sham-operated rats. Neither sympathetic blockade with chlorisondamine (CHLO, 10 mg/kg, s.c.) nor elimination of the pressor effects of VP by use of Brattleboro rats or the VP pressor antagonist resulted in a maximal MAP response significantly different from that in the SAL + DMK-cut group. However, CHLO-pretreatment of Brattleboro rats completely abolished the increase in MAP and HR. It is suggested that the bilateral DMK-cut causes acute hypertension, probably due to the abolition of baroreceptor reflexes by central interruption of neural connections of the nucleus tractus solitarii. It appears that both the increased sympathoadrenomedullary activity and VP release normally contribute to this hypertension; however, either one is sufficient to sustain the elevated blood pressure.

Animals↗