Biomedical subjects

J M Wyss

Publications and source records attributed to J M Wyss.

At least 37 records · Page 2Linked to original sources

PubMed1999

Lifetime treatment with captopril improves renal function in spontaneously hypertensive rats.

Lifetime treatment with captopril prevents the development of hypertension in spontaneously hypertensive rats (SHR). This study tests the hypothesis that compared to untreated hypertensive SHR, captopril-treated SHR display similar diuretic and natriuretic responses to an isotonic saline infusion despite significantly lower arterial pressure. Eight-week-old, male SHR were instrumented with femoral arterial, venous, and bladder catheters. Forty-eight hours later, each rat was infused intravenously with an isotonic saline load (5% of body weight; 0.5 ml/min). Lifetime captopril-treated SHR and untreated control SHR displayed nearly identical natriuretic and diuretic responses to the saline infusion. Thus, although lifetime captopril treatment significantly reduces mean arterial pressure in SHR, renal excretory responses appear to be unaltered. Moreover, histological examination of the kidneys of the lifetime captopril-treated SHR did not reveal significant structural damage in the kidneys at either 8 weeks of age or at 12 months of age. Together, the data suggest that lifetime captopril treatment does not adversely affect renal function and structure in SHR.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1998

Hepatic denervation chronically elevates arterial pressure in Wistar-Kyoto rats.

Several lines of evidence suggest that peripheral osmoreceptors respond to alterations in dietary NaCl by adjusting renal sympathetic nerve activity, but the impact of this reflex on the long-term regulation of mean arterial pressure (MAP) remains unclear. The present study tested the hypothesis that denervation of peripheral osmoreceptors elevates arterial pressure and induces NaCl-sensitive hypertension in normotensive rats. Hepatic denervated and sham-operated Wistar-Kyoto rats were instrumented with telemetry probes for continuous monitoring of MAP and heart rate. After 1 week on a basal (0.6%) NaCl diet, the rats were fed a high (8%) NaCl diet for 2 weeks. On the basal NaCl diet, MAP in hepatic denervated rats was 15+/-1 mm Hg higher than in sham-operated rats. The high NaCl diet did not significantly increase MAP above baseline levels in either denervated or sham-operated rats, but the amplitude of the 24-hour rhythm of arterial pressure increased significantly more in the denervated than in the sham-operated rats. In a second experiment, two similar groups of rats were fed a very low (0.05%) NaCl diet. Mean arterial pressure of the denervated group was significantly higher than that of the sham-operated rats on either the basal or the very low NaCl diet, but the very low NaCl diet did not affect arterial pressure in either group. These results suggest that in the rat, although hepatic osmoreceptors contribute to long-term arterial pressure regulation, they contribute much less to dietary NaCl-induced changes in arterial pressure.

Animals↗

PubMed1997

Pressor and depressor sites are intermingled in the cingulate cortex of the rat.

Electrical stimulation of area infraradiata in the rat evokes transient changes in arterial pressure, but the locations that evoke these responses have not been mapped by neurochemical methods. To localize more specifically the regions of area infraradiata that modify cardiovascular activity, the present study measured cardiovascular responses to localized chemical stimulation of neurons in area infraradiata of urethane-anesthetized rats (n = 21). Microinjections (50-200 nl) of the glutamate agonist D,L-homocysteic acid into area infraradiata evoked both increases and decreases in arterial pressure and heart rate. Injections in the ventral subdivisions of rostral area infraradiata (IRa alpha and IRb alpha) produced cardiovascular responses with the highest probability and greatest magnitude. Of 53 injections in this area, 18 decreased arterial pressure and heart rate, whereas 4 increased arterial pressure and heart rate. In contrast to the results from the ventral subdivision of rostral infraradiata cortex, injections of D,L-homocysteic acid in the dorsal subdivision of rostral infraradiata cortex (IRc alpha) or any of the caudal subdivisions of area infraradiata (IR beta) produced less consistent changes in arterial pressure. To demonstrate that the general anesthesia did not significantly alter the evoked responses in this study, similar injections of D,L-homocysteic acid were made into area infraradiata of unrestrained, conscious rats (n = 10) and the responses were similar to the responses evoked in urethane-anesthetized rats. These results indicate that the ventral subdivisions of rostral area infraradiata (IRa alpha and IRb alpha) are more involved in cardiovascular regulation than other areas of infraradiata cortex (IRc alpha and IR beta), and that both pressor and depressor sites are present in both areas.

Animals↗

PubMed1997

Renal responses to hypertonic saline infusion in salt-sensitive spontaneously hypertensive rats.

In Wistar Kyoto (WKY) and Sprague Dawley rats, high dietary sodium chloride (NaCl) increases natriuretic and diuretic responses to acute isotonic saline infusion, but in NaCl-sensitive spontaneously hypertensive rats (SHR-S), a high-NaCl diet causes negligible increases in natriuretic and diuretic responses. To investigate whether this deficit in sodium and fluid excretion in SHR-S is stimulus (volume)-specific or because of a more generalized alteration in renal function, the present study measured, in SHR-S and Wistar Kyoto rats, natriuretic and diuretic responses to a hypertonic saline infusion (the amount of sodium infused was equal to that infused in a previous, isotonic experiment). Eight-week-old Wistar Kyoto rats, SHR-S, and salt-resistant SHR were given a basal (1%) or high (8%)-NaCl diet for 2 weeks. Intravenous infusion of hypertonic saline increased mean arterial pressure and reduced heart rate in all groups. Baseline sodium excretion was lower in SHR-S compared with salt-resistant SHR with either diet, but after infusion of hypertonic saline, all 6 groups displayed significant increases in sodium and fluid excretion, glomerular filtration rate, and effective renal blood flow (ERBF). The percent-sodium excretion in response to hypertonic saline infusion was slightly, but significantly, lower in SHR-S (compared with salt-resistant SHR) for either the basal or the high-NaCl diet. We conclude that renal responses to hypertonic saline infusion are affected minimally in SHR-S compared with salt-resistant SHR or Wistar Kyoto rats. Therefore, the deficits in renal function observed in SHR-S after volume loading are not reflected in a renal deficit to hypertonic saline challenge.

Animals↗

PubMed1997

Renal function in spontaneously hypertensive rats with insulin-exacerbated hypertension.

This study tests the hypothesis that in spontaneously hypertensive rats (SHR), insulin decreases natriuresis and diuresis and thereby contributes importantly to the hypertensive response to exogenous insulin administration. Seven week old SHR were given daily subcutaneous injections of either insulin (mixture of 5 U/Kg regular and 10 U/Kg NPH) or vehicle (isotonic saline). Within one week of treatment, systolic arterial pressure (SAP) was significantly higher in the insulin, compared to saline, treated SHR (184.2 +/- 2.5 vs. 158.3 +/- 4.0 mm Hg). However, twenty-four hour sodium and fluid excretion and the natriuretic and diuretic responses to an intravenous saline load were not affected either before or after the insulin-induced exacerbation of hypertension in SHR. Insulin treatment did not affect glomerular filtration rate, effective renal blood flow, or fractional excretion of Na+ or fluid. Therefore, our data do not support a major role for sodium and fluid retention in the insulin-induced exacerbation of hypertension in SHR.

Animals↗

PubMed1996

Atrial natriuretic peptide regulation of noradrenaline release in the anterior hypothalamic area of spontaneously hypertensive rats.

In spontaneously hypertensive rats (SHR), high NaCl diets increase arterial pressure and sympathetic nervous system activity by decreasing noradrenaline release in the anterior hypothalamic area (AHA), thereby reducing the activation of sympathoinhibitory neurons in AHA. Atrial natriuretic peptide (ANP) can inhibit the release of noradrenaline, and ANP concentration is elevated in the AHA of SHR. The present study tests the hypothesis that in SHR, local ANP inhibits noradrenaline release from nerve terminals in AHA. Male SHR fed a basal or high NaCl diet for 2 wk and normotensive Wistar Kyoto rats (WKY) fed a basal NaCl diet were studied. In SHR on the basal diet, microperfusion of exogenous ANP into the AHA elicited a dose-related decrease in the concentration of the major noradrenaline metabolite 3-methoxy-4-hydroxy-phenylglycol (MOPEG) in the AHA; this effect was attenuated in the other two groups. In a subsequent study, the ANP-C (clearance) receptor agonist c-ANP was microperfused into the AHA to increase extracellular concentration of endogenous ANP in AHA. c-ANP reduced AHA MOPEG concentration in SHR on the basal NaCl diet but not in the other two groups. These data support the hypothesis that local ANP inhibits noradrenaline release in the AHA and thereby contributes to NaCl-sensitive hypertension in SHR.

Animals↗

PubMed1996

Anterior hypothalamic norepinephrine, atrial natriuretic peptide, and hypertension.

Our laboratory has characterized a model of salt sensitive hypertension, the salt sensitive spontaneously hypertensive rat (SHR-S), in which dietary NaCl supplementation increases blood pressure by reducing norepinephrine release by nerve terminals in the anterior hypothalamic area (AHA), thus reducing activation of sympathoinhibitory neurons in the AHA. This, in turn, results in increased sympathetic outflow and higher blood pressure in the SHR. Two mechanisms have been shown to contribute to this effect: (i) reduced noradrenergic input into AHA via baroreflex pathways and (ii) local inhibition of NE release in AHA by the inhibitory neuromodulator atrial natriuretic peptide (ANP). Studies employing microinjection of a blocking monoclonal antibody to ANP directly into the AHA and the nucleus tractus solitarius (NTS) demonstrated for the first time that endogenous ANP in the brain is functionally active in the tonic control of blood pressure and baroreflex sensitivity in the SHR-S but plays a lesser role in the normotensive Wistar Kyoto (WKY) control. In the WKY, excitation of NTS neurons by baroreflex afferents leads to activation of sympathoinhibitory neurons in NTS and AHA, strong inhibition of sympathetic nervous system outflow, and a decrease in arterial pressure. In SHR-S, brain ANP acts at the levels of the NTS and the AHA to perturb this baroreflex regulatory pathway. ANP tonically activates sympathoinhibitory neurons in the caudal NTS of SHR-S, thereby restraining the rise in arterial pressure, and tonically inhibits baroreflex responsiveness to alterations in blood pressure. Thus ANP appears to act at a number of sites in brain to facilitate the development and maintenance of sympathetically mediated hypertension in the SHR-S model.

Animals↗

PubMed1996

Contribution of the sympathetic nervous system to hypertensive response to insulin excess in spontaneously hypertensive rats.

Our previous studies demonstrate that chronic insulin administration exacerbates hypertension in spontaneously hypertensive rats (SHR). In the present study, we tested the hypothesis that the pressor effect of insulin in SHR is medicated by sympathetic nervous system overactivity. Male SHR (7 weeks old) were given daily subcutaneous injection of insulin or vehicle for 3 days, after which each rat received an intravenous infusion of the peripheral ganglionic blocker hexamethonium. Two days later, in a second experiment, the infusion protocol was repeated with the alpha 2-adrenoceptor agonist clonidine, which more selectively inhibits sympathetic (as compared with parasympathetic) nervous system activity. Insulin treatment for 3 days caused a significant increase in mean arterial pressure (MAP; 164 +/- 2 mm Hg vs. saline control 148 +/- 3 mm Hg), but ganglionic blockade with hexamethonium eliminated the difference in blood pressure (BP) between the insulin-treated and control SHR. Infusion of clonidine significantly reduced MAP in the insulin-treated group to the level of the untreated control SHR, but the infusion did not reduce MAP in the latter group. In a second group of rats, acute administration of prazosin also eliminated the difference in MAP between insulin-treated and control SHR. We conclude that in SHR the sympathetic nervous system contributes importantly to the pressor effect of insulin administration and that this effect may be mediated by the central nervous system.

Adrenergic alpha-Agonists↗

PubMed1996

Atrial natriuretic peptide blunts arterial baroreflex in spontaneously hypertensive rats.

We and other laboratories have reported that arterial baroreflex-mediated control of heart rate is blunted in spontaneously hypertensive rats (SHR) compared with normotensive controls. Recently, we reported that atrial natriuretic peptide (ANP) microinjected into the caudal nucleus tractus solitarii of SHR further blunts this defect. The present study tested the hypothesis that ANP modulates arterial baroreflex-mediated control of sympathetic nervous system activity. Nine-week-old, male SHR (n = 29) and normotensive Wistar-Kyoto control rats (n = 24) were instrumented for microinjection into the caudal nucleus tractus solitarii and for direct measurement of arterial blood pressure, heart rate, and lumbar sympathetic nervous system activity. After urethane- and alpha-chloralose-induced induced anesthesia, arterial baroreflex-mediated control of heart rate and lumbar sympathetic nerve activity was assessed during phenylephrine- (5 to 40 micrograms.kg-1.min-1) induced increases and sodium nitroprusside- (15 to 300 micrograms.kg-1.min-1) induced decreases in mean blood pressure before and after microinjection of ANP (50 ng) or monoclonal antibody to ANP (0.55 micrograms) into the caudal nucleus tractus solitarii. ANP reduced and the antibody enhanced the sensitivity of baroreflex-mediated control of both heart rate and lumbar sympathetic nerve activity in SHR but not in Wistar-Kyoto controls (P < .05). Arterial baroreflex sensitivity was unchanged with control microinjections of vehicle or mouse IgG in SHR. These data suggest that endogenous ANP in the caudal nucleus tractus solitarii may contribute to the development and/or maintenance of hypertension in SHR by blunting baroreflex-mediated control of sympathetic nervous system activity.

Animals↗

PubMed1996

Acute saline infusion decreases norepinephrine release in the anterior hypothalamic area.

Ingestion of a high NaCl diet elevates arterial pressure in spontaneously hypertensive rats, at least in part, by reducing the release of norepinephrine in the anterior hypothalamic area. The mechanism by which dietary NaCl excess alters anterior hypothalamic area norepinephrine release is unknown. Plasma Na+ is slightly elevated after ingestion of a meal; therefore, in the present study we tested the hypothesis that a small increase in plasma Na+ could reduce the release of norepinephrine in the anterior hypothalamic area and elevate arterial pressure. Male spontaneously hypertensive rats were randomized to be fed a diet containing either 1% (basal) or 8% (high) NaCl at age 7 weeks and were maintained on the diets for 2 weeks. Age-matched normotensive Wistar-Kyoto rats received a basal NaCl diet only. All rats were instrumented with a push/pull cannula, and 5 days later, the baseline release of 3-methoxy-4-hydroxyphenyl glycol (the major metabolite of norepinephrine in brain) was measured in awake, freely moving rats. Rats were then challenged with an intravenous infusion (75 microL/min) of hypertonic (2.7%) saline for 20 minutes. In spontaneously hypertensive rats fed a basal NaCl diet, the hypertonic saline infusion elevated mean arterial pressure by 12% and reduced the concentration of the norepinephrine metabolite in the anterior hypothalamic area by 19%; these alterations persisted after termination of the hypertonic saline infusion. Spontaneously hypertensive rats maintained on the high NaCl diet showed greatly reduced arterial pressure and norepinephrine metabolite responses. In normotensive control rats compared with the hypertensive rats fed the basal NaCl diet, the hypertonic saline had considerably less effects on arterial pressure and norepinephrine metabolite levels in the anterior hypothalamic area, and the responses were significantly shorter. Thus, a small elevation in plasma Na+ can reduce the release of norepinephrine in the anterior hypothalamic area. This response is greatly exaggerated in spontaneously hypertensive rats fed a basal (but not a high) NaCl diet, suggesting that a postprandial rise in NaCl could initiate the fall in norepinephrine and thereby contribute to the rise in arterial pressure in spontaneously hypertensive rats ingesting a high NaCl diet.

Animals↗

PubMed1995

Projections from the anterodorsal and anteroventral nucleus of the thalamus to the limbic cortex in the rat.

The present study characterized the projections of the anterodorsal (AD) and the anteroventral (AV) thalamic nuclei to the limbic cortex. Both AD and AV project to the full extent of the retrosplenial granular cortex in a topographic pattern. Neurons in caudal parts of both nuclei project to rostral retrosplenial cortex, and neurons in rostral parts of both nuclei project to caudal retrosplenial cortex. Within AV, the magnocellular neurons project primarily to the retrosplenial granular a cortex, whereas the parvicellular neurons project mainly to the retrosplenial granular b cortex. AD projections to retrosplenial cortex terminate in very different patterns than do AV projections: The AD projection terminates with equal density in layers I, III, and IV of the retrosplenial granular cortex, whereas, in contrast, the AV projections terminate very densely in layer Ia and less densely in layer IV. Further, both AD and AV project densely to the postsubicular, presubicular, and parasubicular cortices and lightly to the entorhinal (only the most caudal part) cortex and to the subiculum proper (only the most septal part). Rostral parts of AD project equally to all three subicular cortices, whereas neurons in caudal AD project primarily to the postsubicular cortex. Compared to AD, neurons in AV have a less extensive projection to the subicular cortex, and this projection terminates primarily in the postsubicular and presubicular cortices. Further, the AD projection terminates in layers I, II/III, and V of postsubiculum, whereas the AV projection terminates only in layers I and V.

Animals↗

PubMed1995

Pressor and bradycardic effects of centrally administered relaxin in conscious rats.

The current study tested the hypothesis that centrally administered relaxin elevates arterial pressure in conscious rats and that this hypertensive effect is mediated, at least in part, by central or peripheral vasopressin. Injection of human relaxin (0.068 or 0.34 microgram in 200 nL artificial cerebrospinal fluid) into the right lateral ventricle of conscious, unrestrained Sprague-Dawley rats caused significant dose-related increases in arterial pressure and decreases in heart rat. The pressor and bradycardic responses to intracerebroventricular injections of relaxin were significantly blunted by pretreatment with either intracerebroventricular or intravenous injection of a vasopressin receptor (V1) antagonist, suggesting that the cardiovascular effects of central relaxin are mediated, at least in part, by V1 receptors in the brain and perhaps also by vasopressin released into the peripheral circulation. Neither intracerebroventricular injection of the vehicle alone nor intravenous injection of relaxin (0.34 microgram) altered arterial pressure or heart rate. In contrast to the above, intravenous injections of relaxin (40 micrograms/kg) elicited pressor and tachycardic responses that were not blunted by pretreatment with either intracerebroventricular or intravenous injection of the V1 receptor antagonist. Together, these data suggest that in the central nervous system relaxin contributes to the regulation of cardiovascular function and that the mechanisms for the cardiovascular effects of central and peripheral relaxin are distinct.

Animals↗

PubMed1995

Contribution of the sympathetic nervous system to salt-sensitivity in lifetime captopril-treated spontaneously hypertensive rats.

OBJECTIVE: To test the hypothesis that, in lifetime captopril-treated spontaneously hypertensive rats (SHR), the sympathetic nervous system contributes importantly to the hypertensive effect of dietary sodium chloride supplementation. METHODS: Male SHR (aged 6 weeks) that had been treated from conception onward with either captopril or vehicle remained on a basal sodium chloride diet or were fed a high sodium chloride diet. After 2 weeks, the rats were subjected to ganglionic blockade and 2 days later, an infusion of clonidine. RESULTS: Lifetime captopril treatment significantly lowered mean arterial pressure in both groups. Intravenous infusion of the ganglionic blocker hexamethonium resulted in a rapid decline in MAP that eliminated the dietary sodium chloride-induced increase in MAP in both groups. Infusion of the central nervous system alpha2-adrenergic receptor agonist clonidine also resulted in a greater reduction in MAP in both groups of SHR that were fed the high (compared with the basal) sodium chloride diet. CONCLUSIONS: In both lifetime captopril-treated and control SHR, the sympathetic nervous system contributes to the pressor effects of a high sodium chloride diet.

Animals↗

PubMed1995

Acute hypertension increases norepinephrine release in the anterior hypothalamic area.

Neurons in the anterior hypothalamic area play an important role in NaCl-sensitive hypertension in spontaneously hypertensive rats, and previous studies have suggested that baroreceptor feedback modifies the activity of these neurons. To test the hypothesis that the release of norepinephrine in the anterior hypothalamic area is modified by arterial baroreceptor reflex feedback and that this reflex release is disturbed in spontaneously hypertensive rats on a high NaCl diet, we used the push-pull technique to measure the release of the norepinephrine metabolite 3-methoxy-4-hydroxy-phenylglycol in the anterior hypothalamic area. Seven-week-old male spontaneously hypertensive and normotensive Wistar-Kyoto rats were placed on a high (8%) or a basal (1%) NaCl diet for 2 weeks. The high NaCl diet elevated mean arterial pressure and greatly reduced basal norepinephrine metabolite levels in the anterior hypothalamic area of the spontaneously hypertensive (but not the control) rats (305 +/- 32 pg/10 min in the rats consuming 1% NaCl and 93 +/- 9 pg/10 min in the rats consuming 8% NaCl). An infusion of tramazoline (an imidizoline that causes long-lasting hypertension) that increased arterial pressure by 25 mm Hg elevated anterior hypothalamic area norepinephrine metabolite concentrations significantly more in the spontaneously hypertensive rats on the 1% NaCl diet (to 392 +/- 46 pg/10 min) than in those on the 8% NaCl diet (to 113 +/- 18 pg/10 min). In contrast, in Wistar-Kyoto rats the tramazoline-induced increase in arterial pressure elevated anterior hypothalamic area norepinephrine metabolite concentrations slightly more in rats on the 8% NaCl diet than in those on the 1% NaCl diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1994

Neurologic consequences of hypertension and antihypertensive drug therapy.

Untreated essential hypertension leads to cardiovascular and renal disease and stroke, but antihypertensive drug therapy effectively reduces these consequences of hypertension. Several studies indicate that hypertension can negatively impact on cognitive function, especially on learning and memory, but the ability of antihypertensive drugs to ameliorate these cognitive dysfunctions is less clear. None of the recent studies convincingly demonstrates that any of the antihypertensive drugs currently in use has a major deleterious effect on cognition in hypertensive patients, but some of the drugs more reliably benefit cognitive function in the hypertensive patient. As a class, the angiotensin-converting enzyme inhibitors most consistently lead to cognitive improvement in the overall hypertensive population, but beta 1-adrenergic receptor blockers and a subset of calcium channel blockers appear to have very similar effects. Animal studies and clinical studies in demented patients suggest that angiotensin-converting enzyme in the cerebral cortex plays a role in normal learning and memory, a finding that provides a theoretic foundation to the beneficial actions of this class of drugs on cognitive function in hypertensive individuals.

Animals↗

PubMed1994

Salt-induced hypertension in normotensive spontaneously hypertensive rats.

Lifetime treatment with oral captopril prevents the development of hypertension in spontaneously hypertensive rats (SHR). We tested the hypothesis that this treatment also prevents the hypertensive response that occurs when untreated NaCl-sensitive SHR are placed on a high NaCl diet. Female SHR were continuously treated with oral captopril before conception and throughout lactation, and the offspring were similarly treated with oral captopril throughout life. At 6 weeks of age, treated male SHR were placed on an 8% (or remained on a 1%) NaCl diet, and systolic arterial pressure, heart rate, and body weight were monitored for 2 weeks. The 8% NaCl diet caused a rapid increase in arterial pressure in the lifetime captopril-treated rats, and 18 days after the initiation of the diet, the mean arterial pressure of this group was 136 +/- 7 mm Hg compared with 100 +/- 2 mm Hg in the 1% NaCl diet rats. The results of a second experiment confirmed the hypertensive effect of the high NaCl diet in lifetime captopril-treated SHR and demonstrated that after 18 days on the diet the dietary NaCl-induced hypertensive response was greater in magnitude in lifetime captopril-treated compared with untreated SHR. The results also demonstrated that lifetime captopril-treated Wistar-Kyoto rats, which are normotensive irrespective of captopril treatment, display no significant increase in arterial pressure when given a high NaCl diet. A third experiment demonstrated that rapidly progressing NaCl sensitivity is also present in female lifetime captopril-treated SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1994

Diurnal blood pressure variation and dietary salt in spontaneously hypertensive rats.

We have previously reported that high dietary salt exposure significantly increases daytime mean arterial pressure in spontaneously hypertensive rats (SHR) but not in normotensive Wistar-Kyoto (WKY) controls. In the present study, we used a telemetry monitoring system to evaluate the effects of high dietary salt exposure on diurnal variation of mean arterial pressure and heart rate in SHR and WKY rats. After implantation of a radio frequency transducer, SHR and WKY rats were maintained on either high (8%) or basal (1%) salt diets. Hemodynamic values were then analyzed for diurnal variation with the use of a nonlinear data-fitting program. After 2 weeks of dietary exposure, high salt-fed SHR had significantly greater 24-hour mean arterial pressure (156 +/- 3 mmHg) than SHR receiving basal (135 +/- 2 mmHg) and WKY rats receiving high (100 +/- 2 mmHg) or basal (100 +/- 1 mmHg) salt diets. Rhythm analysis indicated significant increases in both daytime and nighttime mean arterial pressure during high salt exposure in SHR. In WKY rats, high salt exposure increased nighttime but not daytime mean arterial pressure, with no net effect on 24-hour mean arterial pressure. High dietary salt exposure significantly decreased heart rate in both SHR and WKY rats, and it did not significantly alter the pattern of diurnal blood pressure or heart rate variation. These results indicate that WKY rats manifest an acute sensitivity to salt ingestion but have compensatory mechanisms sufficient to prevent sustained increases in mean arterial pressure; such mechanisms are lacking in SHR.

Animals↗

PubMed1994

Muscle sympathetic nervous system activity in black and Caucasian hypertensive subjects.

OBJECTIVE: To compare muscle sympathetic nerve activity (MSNA) in age- and weight-matched African-Americans and American Caucasians with primary hypertension. DESIGN: Using microneurography, we compared MSNA at rest and in response to cold-pressor testing and handgrip exercise in 13 hypertensive African-Americans and 12 hypertensive American Caucasians. METHODS: All subjects were withdrawn from antihypertensive medications for at least 2 weeks before the study. MSNA was recorded from the left peroneal nerve. RESULTS: Resting MSNA was similar in the Blacks and the Caucasians. Increases in muscle efferent activity, mean arterial pressure and heart rate in response to the cold pressure and handgrip exercise were not significantly different in Black and in Caucasian subjects. CONCLUSION: MSNA, either at rest or in response to certain laboratory stressors, is not different in Black and in Caucasian hypertensive subjects with similar resting blood pressures.

Age Factors↗