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Biomedical subjects

W B Severs

Publications and source records attributed to W B Severs.

At least 73 records · Page 4Linked to original sources
PubMed1981

Urethane anesthesia in rats. Altered ability to regulate hydration.

Anesthesia in rats produced by urethane administered intraperitoneally caused (1) peritoneal fluid accumulation; (2) inability to undergo a renal response to NaCl or water loading, and (3) pronounced hyperosmolality of body fluids without affecting plasma [Na+]. The impairment of the renal function appears not to be due to anesthesia per se, angiotensin, aldosterone, vasopressin or renal nerves. It probably is attributable to osmotoxicity of the mesenteric vasculature. By contrast, urethane administered intravenously evokes a brisk osmotic diuresis without fluid leakage into the peritoneum. Plasma osmolality is still increased. The osmotic toxicity to the mesenteric vasculature, poor renal function and altered composition of body fluids that occur after intraperitoneal urethane may complicate the interpretation of data obtained in rats anesthetized in this manner.

Aldosterone↗
PubMed1981

Endogenous opioid peptide inhibition of the central actions of angiotensin.

Effects of endogenous opioid peptides (leucine5-enkephalin; methionine5-enkephalin; and beta-endorphin) and morphine on isoleucine5-angiotensin II (All)-stimulated increase in plasma vasopressin concentration, blood pressure and drinking behavior were characterized in conscious rats. Plasma vasopressin concentration, drinking frequency and latency were measured 90 sec after intracerebroventricular (i.v.t.) All in animals pretreated with enkephalins, beta-endorphin or morphine, i.v.t. Vasopressin was measured by radioimmunoassay. A consistent dose-related, naloxone-sensitive inhibition of the All-stimulated increase in plasma vasopressin concentration and drinking behavior (frequency) occurred after enkephalins, beta-endorphin or morphine. beta-Endorphin and morphine were longer acting and more potent than enkephalins. In other experiments, All (i.v.t.) pressor activity, drinking volume and latency were measured at hourly intervals after opiates, i.v.t. The All-stimulated increase in mean blood pressure and drinking volume were inhibited by endogenous opioid peptides and morphine, i.v.t. Naloxone prevented opiate inhibition of the All pressor response. Endogenously synthesized opiates may modulate All activity as naloxone potentiated the pressor response and decreased water consumption after All, i.v.t. Continuous i.v. infusion of leucine-enkephalin did not affect All drinking or pressor activity, indicating a central nervous system site of inhibition. Opiate inhibition of the central actions of All appeared independent of sedation; head shakes or wet dog shakes occurred at effective doses of enkephalins. Naloxone did not affect basal blood pressure or plasma vasopressin concentration. Endogenous opioid peptides may modulate the central actions of angiotensin II affecting blood pressure and hydration.

Angiotensin II↗
PubMed1981

Opiate regulation of angiotensin-induced drinking and vasopressin release.

In rats, intracerebroventricular (i.v.t.) administration of endogenous opioid peptides inhibited angiotensin II-stimulated increase in plasma vasopressin concentration and drinking behavior. Naloxone and naltrexone were used to evaluate the effect of opiate receptor blockade on angiotensin drinking behavior. Both antagonists reduced the amount of water consumed and number of animals drinking in response to angiotensin II (i.v.t.). The time to onset of drinking was unaffected. Leucine5-enkephalin inhibition of angiotensin-stimulated release of vasopressin was also studied. Changes in plasma vasopressin concentration with time (5, 45, 90, 150 and 300 sec) were measured after a single i.v.t. injection of angiotensin II (50 ng), with and without pretreatment with leucine5-enkephalin (100 microgram i.v.t.). Vasopressin was measured by radioimmunoassay. The onset of vasopressin release occurred 5 to 45 sec after angiotensin, reaching peak response between 45 to 90 sec. Leucine5-enkephalin did not affect the onset but reduced the peak response to angiotensin (P less than .05). Saralasin, i.v.t., abolished angiotensin-stimulated increase in plasma vasopressin concentration and prevented the residual, but significant, increase in plasma vasopressin concentration in angiotensin-treated rats given enkephalin. It is concluded that angiotensin stimulates release of vasopressin by interaction with specific, saralasin-sensitive, receptors; leucine5-enkephalin inhibits angiotensin release of vasopressin; and an endogenously synthesized opiate ligand(s) may affect angiotensin drinking behavior.

Angiotensin II↗
PubMed1978

Consummatory behavior and urine production after cerebroventricular injection of vasopressin and vasopressin antiserum.

Vasopressin, or vasopressin antiserum, was injected into a lateral cerebral ventricle of conscious rats. These rats were normally hydrated, cellular dehydrated (NaCl loading) or hypovolemic (polyethylene glycol model). Elevation or reduction of vasopressin in cerebrospinal fluid produced no consistent change in consummatory behavior, urine volume or sodium and potassium excretion. These results show vasopressin in cerebrospinal fluid not to be an absolute requirement for maintenance of hydration or for response to acute volume and osmotic stimuli.

Animals↗
PubMed1978

Identification of vasopressin in the subfornical organ region: effects of dehydration.

The subfornical organ (SFO), a neuroendocrine structure implicated in saltwater homeostasis, contains secretory structures histochemically similar to those in the neurohypophysis. Because of these morphological similarities, we compared levels of vasopressin (vp) in the SFO area and the adjacent hippocampal commissure-fornix (HC-F) of normally hydrated and 48 h water-deprived (WD) rats. VP in the SFO region from normally hydrated rats was 44 +/- 5 pg/mg protein, 3.5 +/- 0.4 ng/g wet weight or 3.6 +/- 0.4 pg/SFO. These concentrations increased (P less than 0.05) about twofold after WD. The content of VP, ng/g wet weight, in HC-F was higher (P less than 0.05) than the SFO area and also increased (P less than 0.05) after WD. VP was detected in other fiber tracts, anterior commissure (AC) and fornix (F), but was unchanged by WD. Changes in hormone observed in the SFO and HC-F regions were therefore not part of a generalized increase of VP in the brain, nor can they be ascribed to elevated plasma levels. Thus, VP changes in the SFO region may be functionally significant and related to an SFO endocrine role in hydration. VP in fiber tracts (F, AC) unassociated with the hypothalamo-hypophysial system and unchanged after WD may suggest an unidentified role of this hormone in the central nervous system.

Animals↗
PubMed1978

Drinking in water deprived rats after combined central angiotensin receptor and converting enzyme blockade.

Saralasin, an angiotensin II receptor antagonist, is ineffective in reducing drinking after water-deprivation (WD). Angiotensin III has considerable dipsogenic potency. It may be formed without angiotensin II as an intermediate. To clarify whether angiotensin III formation masks a role for angiotensin in WD, 48 hr WD rats were infused via a lateral cerebroventricle with a) CSF, b) Saralasin, c) SQ 20,881, a converting enzyme inhibitor, or d) Saralasin + SQ. No drug effect on drinking was observed. The results demonstrate that angiotensin III is not required for WD drinking.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1978

Angiotensin II immunohistochemistry of the rat brain.

Immunoreactive angiotensin II (AII) in rat brain is identified histochemically by the unlabelled antibody-enzyme method. Addition of protease inhibitors, phenylmethyl sulfonyl fluoride (PMSF) and ethylenediamine tetra-acetic acid (EDTA), to subzero (-10 degrees C) fixation with propylene glycol and formaldehyde provides reproducible preservation of immunoreactive AII. Synaptic boutons within the brainstem and cerebellum contain immunoreactive AII. The deep cerebellar nuclei have the richest density of AII positive synapses. Other nonneuronal cells such as pinealocytes, pituicytes, and 3rd ventricular tanycytes contain immunoreactive AII. This dual AII localization suggests that both neurons and blood vessels may be involved in the transport of AII to sensitive sites within the rat brain.

Angiotensin II↗
PubMed1977

A microfluorescent PAS method for the quantitative demonstration of cytoplasmic 1,2-glycols.

Fluorescent microspectrophotometry using dichroic mirror vertical epi-illumination of tissue sections stained with the PAS reaction (periodic acid and pararosaniline Schiff reagent) provides a measure of the relative concentration of 1:2 glycols within and between tissue sections. In PAS reacted sections of agarose gel, pararosaniline Schiff fluorescence increases linearly as the concentration of agarose increases (r=0.97, p less than 0.05). The concentration of glycogen within liver as measured by a phenol-based tissue assay is linearly correlated with pararosaniline Schiff fluorescence of formalin fixed liver sections (r-0.87, p less than 0.05). These relationships are unaffected by alcian blue or hematoxylin. Heretofore the amount of color reaction as measured by densitometry at the pararosaniline absorption peak was claimed to be an unreliable indicator of the amount of reactive glycol present in tissue. Our observations indicate that when the concentration of Schiff reagent exceeds an empiric limit relative to available polysaccharides, the Schiff reagent-tissue complex reflects light at the excitation wavelength instead of fluorescing the emission spectra. This can be circumvented by using dilute pararosaniline-Schiff reagent, shorteining the staining period, and lowering the temperature of the staining medium. While routine PAS staining reactions are followed by washing in running water to develop the red color seen with broad spectrum illumination, water development is unnecessary for the dye-tissue complex to fluoresce. The fluorescent emission peak and the maximum excitation peak of both developed and undeveloped pararosaniline-Schiff-reagent-tissue complexes are 645--50 nm and 540--45 nm, respectively. These spectral characteristics are not changed by binding to oxidation products of different glycoproteins or polysaccharides. Intense exposure to room light, but not 100 repetitive short (0.13 s) exposures, causes partial photodecomposition. Quantitative assessment of cytofluorescence requires definition of the optical system used to measure emission. In the microspectrophotometer employed in this study, dichroic mirrors reflect light with variable efficiency depending on wavelength from the light source to the stage, and variably block light reflected or emitted from the specimen, serving as crude barrier filters. These dichroic mirror characteristics are influenced by the exact nature of the optical coating on the surface of each individual mirror. Since the optical coating on the surface of each individual mirror. Since the optical coating of similar mirrors may vary, the properties of individual mirrors must be considered in the interpretation of spectral data and in determining the proper optical conditions for quantification of cytofluorescence.

Animals↗
PubMed1977

Drinking behavior in water deprived rats after angiotensin receptor blockade.

Angiotensin II is a peptide normally present in the bloodstream and central nervous system. Exogenous angiotensin induces drinking which is inhibited by saralasin, a specific receptor antagonist. Administration of saralasin does not reduce endogenously stimulated drinking. Angiotensin is dipsogenic after intravenous or intracerebroventricular infusion, raising the possibility of multiple access routes to the brain. Water deprived rats were given saralasin by both routes simultaneously to block the access of endogenous angiotensin to recentors reached from blood and ventricular cerebrospinal fluid (CSF). Water deprivation increased plasma (Na+), hematocrit, vasopressin content and renin activity but saralasin treatment did not reduce water intake after 30 or 60 min. Therefore, blood or CSF-bore angiotensin does not appear to be an absolute requirement for water deprivation drinking behavior.

Angiotensin II↗
PubMed1977

Norepinephrine-induced reflex bradycardia after central administration of angiotensin II.

Central angiotensin effects may include baroreceptor alterations and/or ventilated, were given angiotensin intravertebrally (10 ng/kg/min), into a lateral cerebroventricle (0.4 microgram/min) or intravenously (10 ng/kg/min). Surgery was completed under methoxyflurane anesthesia; wounds were periodically infiltrated with viscous tetracaine and the methoxyflurane discontinued. The experiments were performed with the brain unanesthetized to optimize detection of an angiotensin effect on the cardioinhibitory component of the baroreceptor reflex. Bradycardia was evoked by norepinephrine injections (2 microgram/kg i.v.). Intraventricular and intravertebral angiotensin increased basal mean blood pressure 16 mm Hg (p less than 0.05); norepinephrine-induced pressor responses and bradycardia were unaffected by the peptide. Intravenous angiotensin did not affect basal blood pressure; a 16 mm Hg increase (p less than 0.05) in the norepinephrine pressor response with no change in bradycardia was observed. Atropine reversed the norepinephrine bradycardia and increased the pressor response in all cats, thus demonstrating the integrity of the reflex. We conclude that centrally administered angiotensin produces no change in the cardioinhibitory reflex to an acute pressor stimulus. The possibility of a peripheral effect of the peptide exists. The hypertensive response observed in the conscious spinal cats after central angiotensin infusions could be due to vasopressin release and/or action of the peptide at cardiovascular sites at high spinal levels.

Angiotensin II↗
PubMed1977

Reduction in plasma vasopressin levels of dehydrated rats following acute stress.

The development of a sensitive radioimmunoassay for plasma arginine vasopressin (pAVP) is described. Using this assay, the levels of vasopressin were determined in the plasma of nondehydrated and dehydrated rats after exposure to ether or acceleration stress. Plasma AVP was also determined in rats following nicotine administration. Nondehydrated rats showed no significant changes in pAVP 1, 2, 5, or 15 min after exposure to ether for 1 min. Dehydrated rats, on the other hand, had significantly reduced pAVP after exposure to ether. One group (180-220 g) showed a decline in pAVP of 27% at 2 min (P less than 0.05) and and 47% at 5 min (P less than 0.001) after stress. In a group of larger animals (350-400 g), pAVP levels were reduced by 55% at 1 min (P less than 0.05) and 72% at 2 min (P less than 0.01) after ether stress. A third group (250-300 g) also had significantly reduced pAVP values of 57% (P less than 0.01) 5 min after ether stress but not at 15 min. Nondehydrated rats which were centriguated at -4.1 Gx for 5, 15 or 120 min showed no significant alterations in pAVP. No decrease in pAVP was observed in dehydrated rats centrifugated for 5 min; after 120 min of centrifugation, mean pAVP was reduced by 40% (P less than 0.02) when compared to be noncentrifugated controls. In contrast to either ether or acceleration stress, nicotine provoked a marked rise (P less than 0.005) in pAVP 10 min after injection. From these results it was concluded that ether or acceleration stress does not evoke an increase in the pAVP levels of rats, and furthermore, in dehydrated rats, these stressors will produce a significant decline in pAVP.

Animals↗