Borderline Hypertensive Rats Research Articles

Effect of immobilization stress on transcriptional activity of inducible immediate-early genes, corticotropin-releasing factor, its type 1 receptor, and enkephalin in the hypothalamus of borderline hypertensive rats.

The effects of immobilization on the expression of immediate-early gene c-fos and nerve growth factor-inducible (NGFI)-B mRNAs, corticotropin-releasing factor (CRF) mRNA, CRF heteronuclear RNA (hnRNA), CRF receptor types 1 and 2alpha mRNA, and enkephalin hn/mRNA were investigated in the hypothalamic paraventricular nucleus of Wistar-Kyoto (WKY) rats and borderline hypertensive rats (BHRs). Rats were deeply anesthetized 0, 30, 60, and 180 min after the beginning of the immobilization session (60 min maximum). BHR paraventricular nuclei displayed slight differences in their resting levels of NGFI-B mRNA and CRF hnRNA, both being significantly elevated compared with those of WKY rats. Conversely, basal levels of enkephalin primary transcript were significantly lower in BHRs. Immobilization, however, induced transient variations in the hybridization signals for all evaluated genes within the paraventricular nucleus (except for CRF 2alpha receptor). Immediate-early gene mRNA levels were higher and more prolonged in BHRs than in WKY rats. This heightened neuronal activation in the BHRs was associated with a more rapid increase in CRF mRNA expression (30 min) compared with that in WKY rats (60 min). It is interesting that a transient rise in CRF hnRNA levels was detected in stressed WKY rats, whereas the BHR group displayed a progressive decline in this transcript, being significantly below resting levels 180 min after the immobilization session. The stress-induced expression of CRF type 1 receptor mRNA was similar in both strains. Moreover, no significant differences were observed for enkephalin hn/mRNA in either strain during the immobilization session. Therefore, the hypothalamic paraventricular nucleus appears to be involved in the functional hyperreactivity of the hypothalamic-pituitary-adrenal and autonomic axes to stress observed in BHRs, which may lead ultimately to a stress-induced hypertensive state.

F002 Platelet NA +/H + exchanger activity is increased in fructose FED borderline hypertensive rats

F002 Platelet NA +/H + exchanger activity is increased in fructose FED borderline hypertensive rats

Vascular and hemodynamic effects of behavioral stress in borderline hypertensive and Wistar-Kyoto rats.

In borderline hypertensive rats (BHR), behavioral stress produces hypertension, which has been attributed to increases in sympathetic nervous system activity and peripheral changes in vascular structure. However, the mechanisms mediating development of stress-induced hypertension have not been well defined. Experiments were designed to determine hemodynamic effects and changes in small mesenteric artery (approximately 300 microns) vascular reactivity in response to 10 days of air-jet stress (2 h/day) in BHR and in Wistar-Kyoto (WKY) rats. The acute stress-induced increase in mean arterial pressure (AP) was impaired in WKY rats compared with BHR on day 1, and habituation developed to the increase in AP in BHR, but not WKY rats. Conversely, WKY rats adapted to the stress-induced tachycardia to a larger extent than BHR. The mechanisms mediating endothelium-dependent relaxation to acetylcholine (ACh) were altered in small mesenteric arteries isolated from WKY rats and BHR after 10 days of air-jet stress. Inhibition of nitric oxide synthase activity had a significantly larger inhibitory effect on ACh-induced relaxation in vessels from stressed compared with control BHR. Also, cyclooxygenase products contributed to ACh-induced relaxation of small mesenteric arteries from stressed WKY rats, but not control WKY rats. Endothelium-independent relaxation to nitroprusside was impaired in vessels from stressed WKY rats, but not stressed BHR. Finally, contraction to phenylephrine was impaired in vessels from stressed BHR, but not WKY rats. In conclusion, changes in vascular reactivity induced by air-jet stress appear to correlate with, and may contribute to, the differential hemodynamic adaptations to stress observed in WKY rats and BHR.

Cardiovascular Effects of the Beta-Carboline FG 7142 in Borderline Hypertensive Rats

Soltis, R. P., V. A. M cGee and M. L. Smith. Cardiovascular effects of the beta-carboline FG 7142 in borderline hypertensive rats. PHYSIOL BEHAV 63(3) 407–412, 1998.—The hypothesis that acute and chronic administration of the benzodiazepine inverse agonist FG 7142 ( N-methyl-β-carboline-3-carboxamide) produces cardiovascular changes similar to those seen during acute and chronic episodes of stress was studied using conscious, unrestrained borderline hypertensive rats (BHR). Chronic intraperitoneal administration of FG 7142 (10 mg/kg; 5 days/week for 8 weeks) failed to alter resting mean arterial pressure or heart rate compared to maturation and vehicle controls. However, chronic administration of FG 7142 prevented the hypertension associated with a high salt diet. Similarly, acute intravenous (I.V.) administration of FG 7142 (10 mg/kg) in BHR rendered hypertensive with a high-salt diet produced a significant reduction in resting mean arterial pressure as well as marked increases in heart rate. Pretreatment with the benzodiazepine receptor antagonist flumazenil (RO 15-1788, 10 mg/kg, i.v.) blocked the tachycardic response but had no effect on the hypotensive effect of FG 7142 administered i.v. in BHR with salt-induced hypertension. Acute administration of FG 7142 (0.1–10 mg/kg, i.v.) in normal BHR produced no significant changes in resting mean arterial pressure and dose-related increases in heart rate. These experiments indicate that, in conscious unrestrained BHR, FG 7142 can elicit changes in heart rate but not the changes in arterial pressure typically associated with stress or anxiety. Therefore, it appears that FG 7142 is of limited use as a pharmacological tool for investigating the cardiovascular effects of acute or chronic stress in BHR.

Role of Neuropeptide Y in Cold Stress-Induced Hypertension

Han, S. P., X. Chen, B. Cox, C.-L. Yang, Y.-M. Wu, L. Naes and T. C. Westfall. Role of neuropeptide Y in cold stress-induced hypertension. Peptides 19(2) 351–358, 1998.—Chronic cold stress (4°C) produced a sustained increase in mean arterial pressure in both normotensive and borderline hypertensive rats (BHR). The high blood pressure in BHRs was significantly reversed by a neuropeptide Y (NPY) Y 1 receptor antagonist suggesting that NPY is involved in mediating stress-induced hypertension. Corresponding increases in adrenal NPY messenger RNA and NPY immunoreactivity were found during the stress; furthermore, chronic cold stress also potentiated the pressor response of rats to a subsequent acute stress test in which NPY has been shown to play a role. These results suggest that chronic cold stress-induced hypertension is mediated by elevated NPY release and vascular tone as a result of increased NPY gene expression and storage.

Exaggerated natriuresis as a candidate intermediate phenotype in spontaneously hypertensive rats.

To determine whether exaggerated natriuresis and exaggerated renal sympathoinhibition during volume loading constitute an intermediate phenotype in spontaneously hypertensive rats. The borderline hypertensive rat, the F1 of a cross between a spontaneously hypertensive rat and a normotensive Wistar-Kyoto rat, is a NaCl-sensitive model of genetic hypertension. In addition to hypertension, borderline hypertensive rats fed 8% NaCl food develop characteristic alterations in regulation of renal sympathetic nerve activity and neural regulation of renal function similar to those in the spontaneously hypertensive rat parent. Like the Wistar-Kyoto rat parent, borderline hypertensive rats fed 1% NaCl food remain normotensive and do not exhibit these alterations in renal sympathetic neural mechanisms. These renal sympathetic neural mechanisms constitute a complex quantitative trait that could represent an intermediate phenotype. A backcross population, developed by mating borderline hypertensive rats with Wistar-Kyoto rats, was fed 8% NaCl food for 12 weeks from age 4 to 16 weeks. Responses to intravenous isotonic saline volume loading (10% body weight/30 min) in 81 backcross rats chronically instrumented for measurement of mean arterial pressure, renal sympathetic nerve activity, and urinary sodium excretion were determined. Mean arterial pressure was 105-180 mmHg and was not correlated to the magnitude either of the decrease in renal sympathetic nerve activity or of the increase in urinary sodium excretion during volume loading. These two aspects of the complex quantitative trait, exaggerated natriuresis and exaggerated renal sympathoinhibition during volume loading, are not part of an intermediate phenotype in spontaneously hypertensive rats.

Early Environmental Influences Can Attenuate the Blood Pressure Response to Acute Stress in Borderline Hypertensive Rats

SANDERS, B. J. AND M. J. GRAY. Early environmental influences can attenuate the blood pressure response to acute stress in borderline hypertensive rats. PHYSIOL BEHAV 61(5) 749–754, 1997.—The objective of this experiment was to test the hypothesis that early environmental influences could affect cardiovascular reactivity to acute stress in borderline hypertensive rats. This study utilized a cross-fostering paradigm in which borderline hypertensive rat (BHR) pups were reared by their natural spontaneously hypertensive rat (SHR) mothers, by an adoptive SHR dam, or by an adoptive Wistar-Kyoto female. Several maternal behavior measures were taken throughout weaning. Cardiovascular responses to acute stress were measured in adult BHR offspring. SHR dams spent significantly more time engaged in arched, as contrasted with passive, nursing behaviors throughout the preweaning period. Although strain of dam had no effect on resting blood pressure or heart rate, BHR reared by WKY dams had a greatly reduced blood pressure response to acute stress compared with BHR raised by either natural or adoptive SHR dams. These results suggest that the expression of cardiovascular characteristics in the BHR can be modified by early environmental influences and support the hypothesis that the expression of the hypertensive phenotype in the BHR is dependent upon information that is conveyed both genetically and environmentally.

Cardiovascular response to stress: baroreflex resetting and hemodynamics.

Borderline hypertensive rats (BHR) were used to test the hypothesis that baroreflex resetting prevents a fall in blood pressure (BP) when cardiac output (CO) is reduced during air-jet stress. Eight-week-old BHR were instrumented with flow probes around the ascending aorta for measuring CO, femoral and jugular catheters were inserted for measurement of arterial pressure and infusion of drugs, and sinoaortic baroreceptors were either denervated (SAD) or left intact. Alternating bolus injections of phenylephrine and sodium nitroprusside were given at baseline and during air-jet stress to assess the baroreflex. Air-jet stress immediately shifted the midpoint of the baroreflex curve for heart rate (HR) to a higher BP levels. When metoprolol was administered during air-jet stress, HR was reduced and CO reverted to prestress levels, but the stress-induced pressor response was not changed. In SAD BHR, air-jet stress caused an elevation of BP that was not different from intact rats. Administration of metoprolol to SAD rats during air-jet stress resulted in a further elevation rather than a reduction in BP. We conclude that the sinoaortic cardiac baroreflex is reset during air-jet stress and that it integrates reflex changes in BP during stress. The arterial baroreflex is not, however, necessary for the initiation or maintenance of the pressor response during stress, nor does it prevent a fall in BP when CO is compromised during stress.

Behavioral stress alters coronary vascular reactivity in borderline hypertensive rats.

Behavioral stress has been proposed to contribute to the occurrence of myocardial ischemia. Objective To investigate the effect of chronic exposure to behavioral stress on the function and structure of the coronary artery of borderline hypertensive rats (BHR). BHR were either exposed to an air-jet stress for 2 h/day for 10 days or kept in their cage for 10 days. After 10 days, hemodynamic measurements in conscious animals were recorded, and their hearts were removed for isolation of a left ventricular coronary artery for functional studies or for fixation by retrograde perfusion for study with scanning electron microscopy. Vascular reactivity was measured in isolated coronary arteries (approximately 250 microm) maintained at an intraluminal diameter of 40 mmHg while the intraluminal diameter was recorded continuously. The resting mean arterial pressure and heart rate in conscious, unrestrained BHR were not altered significantly by exposure to 10 days of 2 h/day air-jet stress. Coronary artery relaxation in response to the endothelium-dependent vasodilator acetylcholine was impaired in rats exposed to the air-jet stress compared with that in controls. An attenuated response to exogenous nitric oxide in coronary arteries from stressed BHR was confirmed by the finding of a reduced sensitivity to nitroprusside, which releases nitric oxide independently from the endothelium. However, relaxation of coronary arteries in response to isoproterenol, which acts independently from nitric oxide, was not altered. Coronary artery contraction in response to endothelin-1 and phenylephrine was not altered in vessels taken from BHR exposed to behavioral stress compared with that in vessels from control rats. Scanning electron microscopy of the endothelial surface of the septal coronary artery showed no difference between vessels from control and stressed BHR. These results indicate that behavioral stress impairs endothelium-dependent and nitric oxide-mediated coronary relaxation, but does not alter alpha1-adrenoceptor or endothelin-1-mediated contraction. By impairing coronary artery vascular relaxation, chronic exposure to behavioral stress may contribute to myocardial ischemia.

Chronic stress induces sensitization in sympathoadrenal responses to stress in borderline hypertensive rats.

The effects of acute foot shock on cardiovascular and sympathoadrenal responses were investigated in chronically stressed borderline hypertensive rats (BHR) and Wistar-Kyoto (WKY) rats. Male BHRs were divided into two groups; the maturation group (Mat) was not stressed, whereas the chronic stress group (AJS) received 8 wk (5 days/wk, 30 min/day) of air-jet stress coupled with immobilization. After chronic stress, the rats were cannulated in the femoral artery and jugular vein. Resting mean arterial pressure (MAP), heart rate (HR), and plasma norepinephrine (NE) levels were higher in the AJS group. In contrast, chronic stress failed to increase basal arterial pressure or HR in WKY rats. In response to acute foot shock, the Mat group had higher MAP increases, at which they plateaued, whereas the AJS rats displayed a progressive decline in MAP. This was associated with higher plasma NE and epinephrine levels but a smaller increase in adrenocorticotropic hormone in AJS versus Mat rats. This hyperactivity in the sympathoadrenal system of chronically stressed BHRs may, in part, account for their mild hypertension.

Cardiopulmonary baroreflex in NaCl-induced hypertension in borderline hypertensive rats.

Borderline hypertensive rats fed an 8% NaCl diet develop increased arterial pressure in association with increased cardiopulmonary baroreflex sensitivity compared with rats fed a 1% NaCl diet. We performed experiments to localize the site of sensitization within the cardiopulmonary baroreflex. To determine whether decreased cardiopulmonary baroreflex sensitivity, as seen in other models of NaCl-induced hypertension, develops later in the course of the disease, we studied an older backcross population derived from borderline hypertensive rats and Wistar-Kyoto rats. Anesthetized borderline hypertensive rats fed 1% and 8% NaCl diets were volume-loaded while right atrial pressure, afferent vagal nerve activity, and renal sympathetic nerve activity were recorded. In 28- to 30-week-old backcross rats fed an 8% NaCl diet, renal sympathetic nerve activity, natriuresis, and diuresis were measured before and during volume loading. Renal sympathetic nerve activity was analyzed with the sympathetic peak detection algorithm. Increases in afferent vagal nerve activity and renal sympathoinhibition were similar in borderline hypertensive rats on either diet during a right atrial pressure rise of 3 mm Hg. In backcross rats, correlations between arterial pressure and renal sympathoinhibition, natriuresis, or diuresis were not found. During volume loading, the peak height of synchronized renal sympathetic nerve discharges decreased while their frequency increased. Attenuated renal sympathoinhibition during acute increases in intravascular volume is not involved in the development or maintenance of NaCl-induced hypertension in borderline hypertensive rats. Renal sympathetic nerve activity decreases because of a reduction in the number of active renal sympathetic nerve fibers.

Norepinephrine Levels in Discrete Brain Nuclei in Borderline Hypertensive Rats Exposed to Compound Stressors

The borderline hypertensive rat (BHR) appears to be an appropriate model for investigating the role of the environment in producing hypertension. Previous studies have demonstrated that the BHR shows chronic blood pressure elevations to both stress and high salt intake. Other studies suggest that interactions between the brain and kidney play an important role in initiating this hypertension. The central noradrenergic system has been implicated in these effects, especially in the hypothalamus. Because exercise has been found to attenuate stress-induced hypertension in the BHR, the current study sought to examine the impact of stressors paired with exercise (salt intake or stress) with those combining stress and high salt. Male BHR were exposed to either control, salt plus stress, salt plus exercise, or stress plus exercise conditions for either 2 or 6 months, beginning at 2 months of age. Following sacrifice, brain nuclei in the brain stem and hypothalamus were removed using the Palkovits micropunch technique. Punches were analyzed for NE content via liquid chromatography with electrochemical detection. Compared with the control condition, chronic salt plus stress led to reductions in NE content, especially in the hypothalamus. Compared with salt plus stress, the exercise conditions were associated with elevated NE levels, especially in the early phases of exposure to the treatment. The possible role of exercise training in preventing a central nervous system trigger from inducing hypertension in the BHR is discussed.

Effect of episodic eucapnic and hypocapnic hypoxia on systemic blood pressure in hypertension-prone rats.

Repetitive episodic (18-24 s twice per minute) hypocapnic hypoxia (HH) administered chronically (7 h/day, 35 days) to Sprague-Dawley or Wistar-Kyoto rats results in a sustained increase in daytime blood pressure (BP). We examined acute and chronic BP response to episodic HH and eucapnic hypoxia (EH) in borderline hypertensive rats [first generation (F1) cross between spontaneously hypertensive and Wistar-Kyoto rats]. We hypothesized that episodic HH and EH would create a greater increase in acute and chronic BP in this breed of rat than in previously studied strains. We also examined neural mechanisms by which BP changes from hypoxia are induced. BP and heart rate were examined acutely in nine F1 rats during baseline, HH, EH, EH with prazosin, and EH with prazosin and atropine. Five groups of male F1 rats were studied after 35-day exposure to the following: Unhandled (n = 8): no treatment; Sham (n = 10): episodic compressed air; HH (n = 14): daily episodic hypoxia (2.7%); EH1 (n = 12); hypoxia 2.9%, CO2 8.4%; and EH2 (n = 11): hypoxia 2.8% and CO2 10.5%. Under acute conditions, HH caused a 34.2-mmHg and EH a 77.9-mmHg increase in mean BP. Prazosin partially blocked the increase in BP. Under chronic conditions, HH caused a 10.3-mmHg increase in daytime mean BP, whereas EH caused a fall in mean BP of 16.6 and 9.3 mmHg in the two separately studied groups. In the F1 rat, acute EH causes an elevation of BP but chronic EH causes a fall in BP. The acute response to EH is not predictive of what occurs after chronic exposure in the hypertension-prone F-1 rat.

Renal Sympathetic Neural Mechanisms as Intermediate Phenotype in Spontaneously Hypertensive Rats

The borderline hypertensive rat, the F1 of a cross between a hypertensive spontaneously hypertensive rat (SHR) and a normotensive Wistar-Kyoto (WKY) rat, is a NaCl-sensitive model of genetic hypertension. In addition to hypertension, borderline hypertensive rats fed 8% NaCl develop characteristic alterations in the regulation of efferent renal sympathetic nerve activity and the neural control of renal function that are similar to those observed in the SHR parent. Like the normotensive WKY rat parent, borderline hypertensive rats fed 1% NaCl remain normotensive and do not exhibit these alterations in renal sympathetic neural mechanisms. These renal sympathetic neural mechanisms constitute a complex quantitative trait that may represent an intermediate phenotype. They have a plausible pathogenetic role in hypertension and are different between SHR and WKY rats. This study evaluated two aspects of this complex quantitative trait, enhanced renal sympathoexcitation with air-jet stress and enhanced renal sympathoinhibition with guanabenz, as a candidate intermediate phenotype. As neither of these aspects was observed in two-kidney, one clip Goldblatt-hypertensive rats, this suggests that the trait is not secondary to hypertension from an acquired cause. In a backcross population (F1 x WKY) fed 8% NaCl for 12 weeks, both enhanced renal sympathoexcitation with air-jet stress and enhanced renal sympathoinhibition with guanabenz cosegregated with the hypertension. These results support renal sympathetic neural mechanisms as an intermediate phenotype in SHR.

Sex chromosomes do not influence renal injury in borderline hypertensive rats.

The present study was undertaken to investigate whether the development of proteinuria in the borderline hypertensive rat (BHR) is influenced by the Y chromosome and to determine if the onset of proteinuria in the BHR is delayed when blood pressure is lowered with enalapril, an angiotensin I converting enzyme inhibitor. Male F1, rats were the first-generation offspring of the mating of spontaneously hypertensive (SHR) females and Wistar-Kyoto (WKY) males and the mating of SHR males and WKY females. At 20 weeks of age, enalapril (125 mg/l) was added to the drinking water. Untreated BHR and enalapril-treated BHR (BHRE) were followed to 90-100 weeks of age. Urine was collected every 10-20 weeks for determination of protein, albumin, and nitric oxide (NO2/NO3) metabolite excretion. Indirect blood pressure in BHR from both crosses was approximately 175 mm Hg from 20 to 90-100 weeks of age. Enalapril lowered blood pressure by about 30 mm Hg, but was ineffective in reducing urinary protein or albumin excretion rates at any age. Urinary excretion of nitric oxide metabolites was similar in all groups at all time periods. There were significant differences in the percent of glomerulosclerosis between the two matings. Based on these results, renal injury in the BHR is not associated with the Y chromosome and can be dissociated from hypertension. Further studies using congenic and transgenic technology will be necessary to identify functions of genes and associations with hypertension in order to understand the kidney disease in this model of hypertension.

Norepinephrine levels in discrete brain nuclei in borderline hypertensive rats exposed to compound stressors

The borderline hypertensive rat (BHR) appears to be an appropriate model for investigating the role of the environment in producing hypertension. Previous studies have demonstrated that the BHR shows chronic blood pressure elevations to both stress and high salt intake. Other studies suggest that interactions between the brain and kidney play an important role in initiating this hypertension. The central noradrenergic system has been implicated in these effects, especially in the hypothalamus. Because exercise has been found to attenuate stress-induced hypertension in the BHR, the current study sought to examine the impact of stressors paired with exercise (salt intake or stress) with those combining stress and high salt. Male BHR were exposed to either control, salt plus stress, salt plus exercise, or stress plus exercise conditions for either 2 or 6 months, beginning at 2 months of age. Following sacrifice, brain nuclei in the brain stem and hypothalamus were removed using the Palkovits micropunch technique. Punches were analyzed for NE content via liquid chromatography with electrochemical detection. Compared with the control condition, chronic salt plus stress led to reductions in NE content, especially in the hypothalamus. Compared with salt plus stress, the exercise conditions were associated with elevated NE levels, especially in the early phases of exposure to the treatment. The possible role of exercise training in preventing a central nervous system trigger from inducing hypertension in the BHR is discussed.

Effects of neonatal growth on adult blood pressures of borderline hypertensive rats.

We conducted this study to test the hypothesis that there are long-term effects of litter-size manipulations during the preweaning period on growth and adult blood pressure of rats. Litter size of genetically homogeneous borderline hypertensive rats, which were produced by cross-mating male Wistar-Kyoto rats with female spontaneously hypertensive rats, was manipulated from 10 to 16 days of age. In addition, a subset of males and females was castrated within the first 30 hours of life. Body weights were measured at several preweaning and postweaning ages, and tail-cuff blood pressures were recorded at 90 days of age. Intact and castrated pups of both sexes that were reared in small (n = 4) litters from 10 to 16 days of age gained nearly twice the weight of animals reared in large (n = 9 to 12) litters during this period. Intact males from small litters had significantly higher adult blood pressures than those from large litters. These long-term effects remained even in groups matched for adult weight and length. Neonatal castration of males completely blocked the consequences of litter-size manipulation on adult blood pressure, suggesting either an organizational or activational role for androgens. Neither intact nor neonatally castrated females exhibited differences in adult blood pressure as a function of litter-size manipulation.

Captopril and stress-induced hypertension in the borderline hypertensive rat

Daily exposure to air-jet stress (AJS) causes sustained elevations of blood pressure in borderline hypertensive rats (BHR). It is known that the renin-angiotensin system is activated during episodes of behavioral stress, and the purpose of this study was to assess the involvement of renin-angiotensin system in the development of stress-induced hypertension in the BHR. Four groups of 8- and 9-week-old rats were studied: they received, respectively, oral captopril and AJS; oral captopril without AJS; AJS without captopril; and neither AJS nor captopril. After 10 days of AJS and captopril conditions, femoral and jugular catheters were implanted for the measurement of mean arterial pressure and pressor responses to norepinephrine and tyramine. Blood samples were collected for the measurement of norepinephrine and plasma renin activity. Ten days of AJS caused a significant elevation of blood pressure in BHR exposed to AJS without receiving captopril but not in those animals given captopril concurrently with AJS. Circulating norepinephrine and blood pressure responses to exogenous norepinephrine and tyramine were similar across the four groups. Plasma renin activity was highest in BHR given captopril, and was significantly elevated during an acute episode of AJS. The renin-angiotensin system may be important in the development of stress-induced hypertension in the BHR.

Telemetered recording of blood pressure and heart rate in different strains of rats during chronic social stress

The role of stress in the etiology of high blood pressure and the biological mechanisms involved are still not clear. We have recently developped a paradigm of chronic social stress based on social instability and cohabitation with females, in which the different neuroendocrine responses to stress can be independently triggered. In this work, we used a telemetry technique to record blood pressure and heart rate chronically in freely moving undisturbed rats to study the influence of chronic social stress on blood pressure and heart rate in normotensive rats (Wistar and Long-Evans) and in Bordeline Hypertensive Rats (BHR). No increase of blood pressure could be seen for one month of social stress in either strain. Wistar and Long-Evans rats were fully sensitive to social pressure, as shown by the changes in body weight, but may lack a specific vulnerability of the cardiovascular system. Conversely, Borderline Hypertensive rats have the genetic predisposition to develop hypertension but do not appear to be sensitive to social stimulations in the present experimental conditions. The experimental protocol used here should allow further investigation of the various possible sources of failure to induce chronic cardiovascular changes by social stress, such as blood pressure measurement techniques, social stress protocols, and genetic aspects of psychobiological and cardiovascular vulnerability to stress.

Swim training alters sympathoadrenal and endocrine responses to hemorrhage in borderline hypertensive rats.

Swim training alters cardiovascular, sympathoadrenal, and endocrine responses to hemorrhage in borderline hypertensive rats (BHR). The effects of 10, 20, and 30% blood volume hemorrhages on cardiovascular, sympathoadrenal, and endocrine function in swim-trained (T; 2 h/day, 5 day/wk for 10-12 wk) and age-matched, untrained, sedentary, control (UT) borderline hypertensive rats (BHR) were assessed. Heart rate (HR) in UT BHR was significantly greater during the baseline (rest) period than T BHR. HR increased slightly from baseline in both groups after 10% hemorrhage but was significantly decreased in both groups after 20 and 30% hemorrhages. The decrease was eliminated by atropine (1 mg/kg iv). Systolic (SBP) and diastolic (DBP) blood pressures decreased significantly after 20 and 30% hemorrhages in both T and UT BHR but were not different between the groups at these times. Plasma norepinephrine levels were significantly increased above baseline after 20 and 30% hemorrhages in UT BHR and were significantly greater in UT BHR than T BHR after 30% hemorrhage. Plasma glucose levels increased significantly after 30% hemorrhage in both groups but were significantly greater in UT BHR than T BHR. Both plasma norepinephrine and plasma epinephrine levels showed strong positive correlations with plasma glucose. After 20 and 30% hemorrhages, plasma insulin levels were unchanged in T BHR but were significantly decreased in UT BHR. Plasma insulin levels were significantly less in UT than T BHR after 30% hemorrhage. These results suggest that swim training alters the effect that hemorrhage exerts on endocrine and sympathoadrenal function in BHR.(ABSTRACT TRUNCATED AT 250 WORDS)