Biomedical subjects

J D Peuler

Publications and source records attributed to J D Peuler.

30 records · Page 2Linked to original sources

PubMed1990

Area postrema and differential reflex effects of vasopressin and phenylephrine in rats.

In normal rats, baroreflex inhibitions of heart rate (HR) and splanchnic but not lumbar sympathetic neural activity (SNA) are greater when mean arterial pressure (MAP) is increased by intravenous infusion of arginine vasopressin (AVP) compared with phenylephrine (PE) or methoxamine. In normal rabbits, baroreflex inhibitions of HR and lumbar and renal SNA are all greater when MAP is increased by AVP vs. PE. The differential reflex bradycardic and renal sympathoinhibitory effects of AVP vs. PE in rabbits require an intact area postrema. To determine whether differential reflex effects of AVP vs. PE in rats is selective for HR or inclusive of renal SNA and to examine the role of the rat area postrema in such action, we monitored HR and renal SNA in normal (sham operated, n = 8) and area postrema-lesioned (APX, n = 8) rats under chloralose anesthesia during slow increases in MAP (less than 0.3 mmHg/s; 3 min) induced intravenously by AVP (0-16 mU.kg-1.min-1) and by PE (0-8 micrograms.kg-1.min-1). Reflex inhibition of HR (-delta betas.min-1.delta mmHg-1) was greater when MAP was increased by AVP vs. PE in normal rats (-2.7 +/- 0.5 vs. -1.7 +/- 0.1, P less than 0.05), and this difference was absent in APX rats (-2.5 +/- 0.5 vs. +/- -2.2 +/- 0.4). Similarly, maximum bradycardia (-delta beats/min) by AVP vs. PE was greater in normal rats (-64 +/- 8 vs. -48 +/- 7, P less than 0.05) but not in APX rats (-53 +/- 5 vs. -52 +/- 6).(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1989

Altered peripheral noradrenergic activity in intact and sinoaortic denervated Dahl rats.

Development of salt-induced hypertension in Dahl salt-sensitive (S) rats is dependent on sympathetic overactivity which may be partially related to arterial baroreflex dysfunction and, therefore, is regionally selective. Our first experiment was designed to determine which regions have elevated sympathetic activity in Dahl S compared with Dahl salt-resistant (R) rats. Weanling (4-week-old) female Dahl R and S rats were fed low or high salt diets (0.13% and 8% NaCl) until 10 weeks of age. Norepinephrine (NE) synthesis was blocked with alpha-methyl-p-tyrosine, and the fractional decline of NE concentration was measured in various tissues. Dahl S rats with increases in both arterial pressure and left ventricular weight demonstrated increased NE turnover in the sinoatrial node, the atrial appendages, the cardiac ventricles, and the renal cortex. In all of these tissues except the cardiac ventricle, increases were associated with high salt intake. Our second experiment was designed to test if arterial baroreflex dysfunction could account for regional increases in sympathetic activity. Separate groups of Dahl R and S rats fed high salt were subjected to either sham surgery or sinoaortic baroreceptor denervation 1 week prior to turnover determinations. Sinoaortic baroreceptor denervation abolished differences in NE turnover between salt-fed Dahl R and S rats in the cardiac sinoatrial node and the atrial appendages, but not in the cardiac ventricles and the renal cortex. Sinoaortic baroreceptor denervation also abolished differences between salt-fed Dahl S and R rats in the spleen but not the duodenum.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1989

Central noradrenergic activity in intact and sinoaortic denervated Dahl rats.

Lesions in forebrain areas richly innervated by noradrenergic terminals and involved in cardiovascular function reduce or prevent hypertension in the Dahl salt-sensitive (S) rats fed a high (H) salt diet. This led us to examine two questions. (1) Is the noradrenergic activity altered in discrete forebrain and brainstem areas of SH rats? (2) Are these changes in noradrenergic activity eliminated by sinoaortic denervation (SAD)? Studies were done in 10-week-old female SH and Dahl salt-resistant (RH) rats. Half of the rats in each group had SAD surgery 1 week prior to study. An index of norepinephrine (NE) turnover was determined by measuring the decline in tissue NE concentration 8 h after administering alpha-methyl-p-tyrosine, a NE synthesis blocker, to animals from each of four groups: sham-RH, SAD-RH, sham-SH, and SAD-SH (n = 18-20 per group). Various discrete brain areas were obtained using the "punch technique." In SH rats the index of NE turnover was increased in the median preoptic nucleus and decreased in the paraventricular nucleus compared with RH rats regardless of SAD. In contrast, in SH rats the index of NE turnover was increased in the supraoptic nucleus and locus ceruleus compared with RH rats; however, SAD-RH had greater turnover of NE at these sites than SAD-SH. In summary, changes in noradrenergic activity in the median preoptic nucleus and the paraventricular nucleus may be related to genetic predisposition to hypertension in SH rats. In contrast, changes in the locus ceruleus and the supraoptic nucleus of SH rats may be related to impaired baroreflexes and thereby contribute to hypertension.

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PubMed1989

24-hour blood pressure recordings in Dahl rats on high- and low-salt diets.

The goal of this study was to determine if the baroreflex abnormality previously shown in Dahl-sensitive (DS) rats would increase blood pressure and heart rate (HR) variability. Mean arterial pressure (MAP) and HR were sampled every 2 s for 24 h from Dahl-resistant (DR) and DS rats on low- and high-salt diets (n = 12-13 in each group). MAP +/- SD was significantly elevated in the DS rats on high-salt diets (DSH); the SD of MAP in the DSH rats was also significantly higher compared with similar measurements in rats on high-salt diets (DRH) and DS rats on low-salt diets (DSL) when SD was divided by MAP. MAP was higher at night than during the day in the DSH rats. In contrast, HR and HR variability were not significantly different between the groups. The baroreflex control of HR, determined by means of graded injections of phenylephrine, was least in the DSH rats and increased, respectively, with DSL rats, DRH rats, and DR rats on low-salt diets. There was no significant correlation between the baroreflex control of HR and MAP or the SD of MAP in the DSH rats, suggesting that there is not a simple relationship between baroreflex gain and the overall behavior of MAP in DSH rats.

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PubMed1989

Aggravation of salt-induced hypertension in Dahl rats by 2% supplemental dietary calcium.

There is considerable interest in the antihypertensive potential of supplemental dietary calcium in salt-sensitive hypertension. Previously we reported that very high dietary calcium (4.0% vs. 0.4%) lowers mean arterial pressure in Dahl salt-sensitive (DS) hypertensive rats. However, we have recently observed that more moderate calcium supplementation (2.0% vs. 0.4%) increases mean arterial pressure in DS rats. To further evaluate the pressor action of 2.0% versus 0.4% calcium, we tested for effects of 2.0% calcium in female DS rats fed low (0.2%), moderate (1.0%), and high (2.7%) sodium and in Dahl salt-resistant (DR) rats fed high sodium from 6 to 12 weeks old (n = 10-13 rats per group). At 12 weeks, 2.0% calcium increased mean arterial pressure and the cardiac ventricular weight/body weight ratio in DS rats fed high sodium (p less than 0.05) but not in DS rats fed low or moderate sodium or in DR rats fed high sodium. Ganglionic blockade decreased mean arterial pressure in all groups but failed to abolish or attenuate the difference in mean arterial pressure between high sodium-fed DS rats on 2.0% and 0.4% calcium diets. In the same DS rats fed a high sodium diet, 2.0% calcium increased systemic pressor responsiveness to graded norepinephrine administration after ganglionic blockade. Thus, 2.0% supplemental calcium intake enhances salt-induced hypertension in DS rats. This prohypertensive action of 2.0% calcium is dependent on a critically high level of between 1.0% and 2.7% sodium in the diet.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1989

Renal sympathetic nerves attenuate the natriuretic effects of atrial peptide.

Low frequencies of renal sympathetic nerve stimulation increase renal tubular sodium reabsorption without causing renal hemodynamic changes. We tested the hypothesis that the natriuretic responses to synthetic atrial peptides (atriopeptin III [APIII], 24 amino acids) are modulated by the renal tubular actions of the renal nerves. Responses to intravenous infusions of APIII (0.5 and 2.0 micrograms/kg/min) were examined in three groups of chloralose-anesthetized rats. Bilateral renal function studies were done in all three groups in which the right kidney was denervated and the left kidney was either left innervated (group I, n = 10) or the distal portion of the transected left renal nerves was stimulated at 15 V, 1 msec, and 0.5 Hz (group II, n = 8) or 1.0 Hz (group III, n = 8). In groups I, II, and III, diuretic and natriuretic responses to APIII were significantly (p less than 0.05) less in the kidneys with intact innervation or low-frequency (0.5 and 1.0 Hz) renal nerve stimulation than in the denervated kidneys. In conclusion, renal excretory responses to APIII are substantially modulated by the renal tubular actions resulting from low-frequency renal nerve stimulation. We speculate that the decrease in renal excretory responses to atrial peptides in pathophysiologic states such as congestive heart failure, nephrotic syndrome, and cirrhosis may result in part from an increase in the prevailing level of renal sympathetic nerve activity.

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PubMed1987

High calcium diet reduces blood pressure in Dahl salt-sensitive rats by neural mechanisms.

We tested the hypothesis that high dietary calcium attenuates hypertension in Dahl salt-sensitive rats by neural as opposed to vascular mechanisms. Four-week-old Dahl salt-sensitive rats were fed a high salt diet (3.3% sodium) with either high (4.0%; n = 21) or normal (0.4%; n = 21) calcium content until they were 10 to 11 weeks old. Total plasma calcium concentration was increased and plasma phosphorus concentration was decreased by the high calcium diet. At 10 weeks, food intake and intestinal absorption of sodium were not altered by the high calcium diet. There were three major observations. First, mean arterial pressure was lower in awake rats fed a high versus normal calcium diet (137 +/- 7, n = 11, vs 165 +/- 6 mm Hg, n = 10, respectively; p less than 0.05). This pressure difference was dependent on intact autonomic transmission, since ganglionic blockade eliminated the significant difference between pressures in rats fed high (78 +/- 5 mm Hg) and normal (85 +/- 6 mm Hg) calcium diets. Second, high calcium intake augmented baroreceptor reflex inhibition of renal sympathetic nerve activity and heart rate during ramp increase in arterial pressure produced by infusion of phenylephrine. Reflex suppression of renal sympathetic nerve activity was twofold greater in rats fed the high (vs normal) calcium diet (-2.79 +/- 0.25 vs -1.34 +/- 0.14% delta/delta mm Hg, respectively; n = 9 rats per group; p less than 0.05). Third, high calcium intake did not attenuate vascular responsiveness, since pressor responses to norepinephrine and angiotensin II did not differ between rats fed high and normal calcium diets after ganglionic blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1985

Sodium balance and blood pressure during high sodium ingestion in spontaneously hypertensive and Wistar Kyoto normotensive rats.

Objectives of this study were to compare natriuretic capability and arterial pressure elevation at high Na+ ingestion in male spontaneously hypertensive (SH) and normotensive Wistar Kyoto (WKY) rats at the young adult age of 16-19 weeks. 10 SH and 10 WKY male rats at this age were surgically implanted with arterial catheters. After a period of 10 days on low nutritionally adequate Na+ intake they were fed a high Na+ diet for a period of 1 week. Na+ retention (intake-output) on the high Na+ diet was substantial, but similar in both groups of rats. None of the animals displayed meaningful elevation of arterial pressure. Thus, the functional capacity of the young SH rat to excrete Na+ during excessive ingestion without elevation of blood pressure seems adequate as compared to normotensive rats, at least within the age range of 16-19 weeks.

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PubMed1982