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Biomedical subjects

B J Sanders

Publications and source records attributed to B J Sanders.

At least 37 records · Page 2Linked to original sources
PubMed1990

Dam strain affects cardiovascular reactivity to acute stress in BHR.

The effect of maternal strain on reactivity to acute stress was studied in F1 reciprocals produced by crossing the spontaneously hypertensive rat (SHR) with its normotensive progenitor, the Wistar-Kyoto (WKY). This F1 generation, known as the borderline hypertensive rat (BHR), is genetically predisposed to develop hypertension in response to chronic stress or high dietary sodium. Reciprocals, considered to be genetically equivalent aside from sex-linked traits, differ in strain of dam during intrauterine and preweanling development. At 17 weeks of age, reciprocal F1 males did not differ in open-field behavior (squares crossed, rearings, and defecation measured over 3 days in 15-min sessions) or in home-cage measurements of mean arterial pressure (MAP) and heart rate (HR). However, different patterns of cardiovascular reactivity were displayed to transfer and footshock. While WKY-mothered rats reacted with graded pressor responses, SHR-mothered rats responded maximally to transfer, showed no additional increase to footshock, and maintained peak responding after footshock was terminated. Such reactivity differences may mediate the impact of environmental variables on the genetic disposition to hypertension.

Animals↗
PubMed1989

Haemodynamic responses to conflict stress in borderline hypertensive rats.

Chronic exposure to a shock-shock conflict paradigm (2 h/day, 5 days/week for 12 weeks [1]) produces hypertension in the borderline hypertensive rat (BHR), a cross between the spontaneously hypertensive rat (SHR) and the Wistar-Kyoto rat (WKY). The purpose of the present study was to characterize the regional haemodynamic responses which take place during conflict-stress. A pulsed Doppler flowmeter and miniature probes implanted on the left renal and superior mesenteric arteries and the abdominal aorta were used to record changes in regional flow velocity. Recording of mean arterial pressure (MAP) allowed changes in regional resistance to be calculated. The first conflict session produced intense splanchnic and renal vasoconstriction and hindquarter vasodilation. Pressor responses were moderate. A second group of BHRs was studied during conflict sessions 17-18, prior to the development of hypertension. This group exhibited faster habituation to the stress than the group studied during the first conflict session: MAP and mesenteric resistance returned more rapidly towards pre-stress levels. Relative to naive control rats, this group exhibited a larger peak MAP and less tachycardia in response to a neutral stressor (air-jet stress) and a smaller reduction in renal resistance in response to ganglionic blockade. These data suggest that in this model, pressure load per se is moderate. More attention should be directed towards the role of trophic effects of the neurohumoral factors responsible for the pronounced constriction of splanchnic and renal vasculature in producing hypertension.

Analysis of Variance↗
PubMed1989

Lesions of the anteroventral third ventricle and development of stress-induce hypertension in the borderline hypertensive rat.

The anteroventral third ventricle (AV3V) region plays a critical role in the pathogenesis of many forms of experimental hypertension. The present study sought to determine whether the integrity of this area was necessary for the development of stress-induced hypertension in the borderline hypertensive rat (BHR). Male BHRs were assigned to three groups at 8 weeks of age: 1) AV3V lesion, 2) sham lesion, and 3) maturation control. BHRs with AV3V and sham lesions were exposed to 12 weeks of conflict stress (2 hr/day, 5 days/wk). At the end of the conflict protocol period, direct measurement of resting mean arterial pressure indicated that BHRs with sham lesions had significantly higher blood pressure (153 +/- 2.9 mm Hg) than rats with AV3V lesions (126 +/- 5.2 mm Hg) and maturation control rats (133 +/- 4.3 mm Hg). Although AV3V lesions prevented stress-induced hypertension in BHRs, these rats were still capable of transiently raising blood pressure. Specifically, the results also indicate that BHRs with AV3V lesions showed greater increase in blood pressure in response to an electric foot-shock paradigm. This study suggests a critical role for this forebrain region in the production of stress-induced hypertension in genetically predisposed animals.

Animals↗
PubMed1989

Lesions of the anteroventral third ventricle prevent salt-induced hypertension in the borderline hypertensive rat.

Many forms of experimental hypertension depend on the integrity of the periventricular tissue surrounding the anteroventral third ventricle. The current investigation examined the extent to which this forebrain area is necessary for the elaboration of salt-induced hypertension in the borderline hypertensive rat. Eight-week-old male rats were given either electrolytic lesions of the anteroventral portion of the third ventricle region or sham lesions. All rats were then placed on a high salt diet (8% NaCl) for 10 weeks. At the conclusion of this dietary period, direct measurement of resting mean arterial pressure revealed that borderline hypertensive rats with lesions of the anteroventral portion of the third ventricle had significantly lower blood pressure (128.4 +/- 5.1 mm Hg) compared with sham-operated rats (148.1 +/- 4.1 mm Hg).

Analysis of Variance↗
PubMed1989

Bilateral renal denervation can prevent the development of stress-induced hypertension in the borderline hypertensive rat.

The borderline hypertensive rat (BHR) shows large blood pressure responses to either stress or a high salt diet. Since the renal nerves have been shown to play a role in several animal models of hypertension, the current study sought to determine the effect of bilateral renal denervation on the development of stress-induced hypertension in the BHR. BHR were deprived of renal nerves under ether anesthesia after either 5 or 11 weeks of daily 2-hour stress sessions. Additional BHR received sham surgery. Unstressed BHR, age-matched to stressed groups, received denervation or sham surgery. Following a 3 week recovery period, the protocol (stress or no stress) was continued for 10 additional weeks. Tail cuff systolic blood pressures were obtained weekly. BHR stressed for 5 weeks prior to denervation failed to develop hypertension in response to continued stress. Although BHR stressed for 11 weeks prior to denervation showed a temporary reduction in pressure following denervation, blood pressure returned to the hypertensive levels of sham-operated controls after several weeks. Thus, there may be a critical period during which the renal nerves are necessary for the expression of stress-induced hypertension in the BHR. These observations are discussed in relation to the effects of renal denervation on hypertension in various animal models.

Animals↗
PubMed1988

The borderline hypertensive rat: a model for studying the mechanisms of environmentally induced hypertension.

The borderline hypertensive rat (BHR) is a first-generation cross between the spontaneously hypertensive rat and the normotensive Wistar-Kyoto rat. The BHR develops frank hypertension when chronically stressed or when fed a high-sodium diet. Stress-induced hypertension can be blocked by exercise. The role of the central nervous system and kidney in hypertension development in this model is discussed.

Animals↗
PubMed1988

Effects of adrenal demedullation on stress-induced hypertension and cardiovascular responses to acute stress.

Because chronic infusions of adrenalin (A) produce hypertension in rats, it has been suggested that A is a mediator of stress-induced hypertension. In order to test the hypothesis that lowering A will attenuate stress-induced hypertension, rats who had their adrenal medullae removed (ADM) and sham-operated controls were subjected to chronic stress. All subjects were offspring of a cross between spontaneously hypertensive and Wistar-Kyoto rats. Prior to chronic stress, systolic pressures were the same in the two groups. The stress consisted of 60 2-h sessions of shock-shock conflict during 18 weeks. After conflict stress, the rats were implanted with arterial catheters and allowed two days to recover. The resting mean arterial pressure (MAP) was 141.2 mmHg in the ADM group and 142.3 mmHg in the Sham group. Cardiovascular responses to acute stress were then examined. The rats were transferred to a test-box and subjected to pulsed foot shocks (0.5-s duration, 5-s intervals) for 5 min. The MAP increase after transfer was 22.3% in the ADM and 4.2% in the Shams (P less than 0.001). After termination of the shocks, the MAP was elevated 22.2% above baseline in the ADM and 8.1% in the Shams (P less than 0.02). Five minutes after foot shocks the MAP increase was 21.6% in the ADM and 7.2% in the Shams (P less than 0.02). Adrenal demedullation was effective in attenuating plasma A during stress and reduced the plasma noradrenaline response. Therefore, the larger pressor responses of the ADM group seem to result from attenuation of beta-adrenoreceptor-mediated dilation of skeletal muscle vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1988

Cardiovascular and renal responses to stress in borderline hypertensive rat.

Wistar-Kyoto (WKY) and borderline hypertensive rats (BHR) were exposed to either a normal or high-sodium chloride (NaCl) diet for 8 wk. Cardiovascular and renal data were collected from arterial and bladder catheters, respectively, in conscious animals during control and stress (aversive classical conditioning) sessions. Results indicated that BHR on a high-NaCl diet exhibited no increase in blood pressure in response to stress compared with BHR on a normal diet. A high-NaCl diet diminished the recovery of blood pressure to base line during stress in WKY compared with normal NaCl controls. Also, a high-NaCl diet and stress interacted in the BHR to decrease sodium excretion and renal plasma flow during stress compared with the control session (3.8 vs. 4.8 mueq.min-1.100 g body wt-1; 3.6 vs. 4.0 ml.min-1. 100 g body wt-1, respectively). Finally, increased dietary NaCl blunted the norepinephrine response to stress in WKY but not in BHR (263 vs. 767 pg/ml). These data suggest that the interaction of genetic and environmental factors are important variables for the development of hypertension.

Animals↗
PubMed1987

Hypertension produced by a high sodium diet in the borderline hypertensive rat (BHR).

The effect of high dietary sodium (8%) on blood pressure in spontaneously hypertensive (SHR), borderline hypertensive (BHR), and normotensive Wistar-Kyoto (WKY) rats was determined weekly by tail cuff plethysmography for one week of baseline and four weeks of diet. After 4 weeks, significant elevations in systolic blood pressure were found in SHR and BHR groups, but not in WKY. BHR studied an additional 4 weeks showed a further progression of hypertension, reaching levels nearly equal to control SHR. Direct measurement of arterial pressure in conscious animals in their home cage confirmed the elevation in pressure in both SHR and BHR groups. Metabolic studies revealed that the high sodium diet reduced body weight in SHR and BHR strains, but not in WKY. Although both urinary volumes and sodium excretion values were significantly lower in SHR and BHR compared with WKY, this effect disappeared when adjustments for body weight were made. Plasma norepinephrine determinations revealed a significant response to cold stress in all groups. Plasma epinephrine was elevated in all strains in response to cold stress; however, a consistent statistical elevation was seen only in WKY. The BHR is discussed as a model for determining the triggers responsible for environmentally-induced hypertension.

Animals↗
PubMed1986

The effects of intracerebroventricular injection of clonidine on conditioned pressor and adrenergic responses in rats.

Studies from this laboratory have shown that the first filial offspring of female spontaneously-hypertensive rats and male Wistar-Kyoto (WKY) normotensive rats develop stress-induced hypertension. The present study sought to examine the effects of intracerebroventricular administration of clonidine (8 micrograms) on cardiovascular and sympathoadrenal responses to aversive classical conditioning in these borderline hypertensive rats (BHR) and in normotensive WKY control rats. Clonidine caused significant reductions in resting arterial pressure, vascular resistance, heart rate and concentrations of epinephrine (E) in plasma for both hypertensive and normotensive rats. Central administration of normal saline to control rats of each strain did not alter basal cardiovascular or sympathoadrenal function. The presentation of a conditioned stimulus (CS) elicited a significant increase in arterial pressure and total peripheral resistance in hypertensive rats treated with saline and clonidine and in normotensive rats treated with saline. In contrast, normotensive rats treated with clonidine showed no increases in arterial pressure or vascular resistance following the onset of the conditioned stimulus. The aversive conditioning session instigated significant increases in the concentrations of norepinephrine (NE) and E in plasma in saline-treated rats. Hypertensive and normotensive rats treated with clonidine-showed a blunted increase in plasma concentrations of NE and E during this period; however, concentrations of E in hypertensive rats increased significantly from the baseline period after injection. These data suggest that an abnormality in central alpha 2-adrenoceptor-mediated inhibition of sympathoadrenal discharge and sympathetic vasomotor tone may predispose the hypertensive rat to develop stress-induced hypertension.

Animals↗
PubMed1986

Changes in cardiac output and vascular resistance during behavioral stress in the rat.

Normotensive Wistar-Kyoto (WKY) rats and borderline hypertensive rats (BHR) were exposed to aversive classical conditioning procedures and chronically instrumented with arterial catheters and electromagnetic flow probes around the ascending aorta. After postoperative recovery, hemodynamic measurements and blood samples were obtained from conscious animals at rest and during aversive conditioning. The cardiovascular response to the behavioral stress consisted of a significant increase in mean arterial blood pressure, total peripheral resistance index, cardiac index, heart rate, and aortic dP/dt for both strains. However, the elevated vascular resistance seen in the BHR resulted in a significantly greater increase in mean arterial blood pressure (21 mmHg) compared with the WKY rats (14 mmHg). In addition, the BHR showed a significantly (P less than 0.05) greater plasma norepinephrine concentration (760 +/- 99 pg/ml) in response to the stress than did the WKY rats (559 +/- 53 pg/ml). These data suggest that an increase in cardiac output, elevated vascular resistance, and increased sympathetic drive may contribute to the development of stress-induced hypertension in this animal model.

Animals↗
PubMed1985

Blood pressure and heart rate responses to environmental stress in the spontaneously hypertensive rat.

Blood pressure and heart rate responses of the spontaneously hypertensive rat (SHR) and the Wistar-Kyoto rat (WKY) to mild restraint and tone-shock pairings were compared during a pre-stress, aversive conditioning and post-stress period, after five previous days of exposure to the paradigm. Although SHR and WKY showed similar responses to the onset of the pre-stress period, SHR showed significantly larger blood pressure responses following the onset of the conditioning than WKY. Furthermore, WKY showed a significant blood pressure and heart rate reduction during the conditioning session which was absent in the SHR. During the post-stress period, the blood pressure of SHR remained significantly elevated compared to their home cage rest values, but the blood pressure of WKY returned to basal levels. It is concluded that while the SHR is more reactive than the WKY to stimulus onset, the major source of between-strain differences after 20 min relates to differences in adaptation to continued environmental stimulation. This can lead to exaggerated estimates of physiological reactivity of the SHR, and is supportive of Folkow's view that SHR are both hyperreactive and show more prolonged defense reactions.

Animals↗
PubMed1985

Cardiovascular and sympathoadrenal responses to stress in swim-trained rats.

Chronic exposure to swim stress (i.e., training) is associated with functional adaptations of the cardiovascular system. On the other hand, repeated exposure to tail shock, an emotional stress, often results in deleterious changes in resting blood pressure and myocardial pathology. We hypothesized that the pathological adaptation following chronic exposure to tail shock was associated with a larger acute physiological response compared with swim stress. Therefore, acute responses to swim and shock stress were compared. A second concern of this study examined the extent to which adaptation to swim training influences responses to predictable tail shock stress. The cardiovascular and sympathoadrenal responses to swim stress, using 1% body wt attached to the tail, were compared with predictable tail shock (0.2-0.4 mA intensity, 1-s duration, 1/min) in two groups of Long-Evans male rats. In the first, 11 rats were studied following 5-7 wk of swim training, consisting of daily 1-h sessions of swimming with 2% body wt attached to their tails. They were compared with an age-matched nontrained (NT) group (n = 8). During swimming, the trained animals showed significantly lower heart rate (387 +/- 10 vs. 449 +/- 18 beats/min) and significantly lower lactate (0.9 +/- 0.09 vs. 2.0 +/- 0.24 mmol/l), epinephrine (332 +/- 57 vs. 739 pg/ml), and corticosterone (32 +/- 10 vs. 62 +/- 9 micrograms/dl) responses. Systolic and diastolic blood pressures were elevated in swim stress by the same degree in trained (167/110 mmHg) and NT (177/116 mmHg) rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1975

Palytoxin: effects on contractility and 45Ca2+ uptake in isolated ventricle strips.

Palytoxin (PTX) inhibited phasic tension production and initiated tonic contracture in isolated paced ventricle strips at concentrations greater than 10(-10) M. PTX-induced contracture was associated with increased 45Ca2+ uptake. PTX-induced additional 45Ca2+ uptake was completely blocked by 2 mM La3+. All observed PTX effects were enhanced by elevation of [Ca2+] o from 1.9 to 6 mM and this threefold increase in [Ca2+] o resulted in a threefold increase in isotope-determined Ca2+ uptake in presence of 10(-8) M PTX. It is concluded that the observed effects of PTX could be mediated by an increase in calcium permeability of myocardial cells.

Acrylamides↗
PubMedDate not supplied

Exercise training attenuates stress-induced hypertension in the rat.

The ability of exercise training to block the generation of hypertension produced by chronic stress in the borderline hypertensive rat was tested. Twenty-three male borderline hypertensive rats, F1 offspring of spontaneously hypertensive and Wistar-Kyoto rats, were divided into three groups. Two groups (8 rats per group) were subjected to 2 hours of daily, predictable, uncontrollable tail shock for 12 weeks. One of these groups was also given 2 hours of daily swim stress (exercise trained). A third group served as a maturation control and received neither intervention (n = 7). After 12 weeks of stress, direct recording of blood pressure verified the pattern observed with tail cuff: shock only group, 180/118 +/- 3/3 mm Hg; exercise-trained and shocked group, 166/108 +/- 4/2 mm Hg; and control group, 160/98 +/- 6/4 mm Hg (mean +/- SEM). Systolic and diastolic blood pressures in the shock only group were significantly higher than in both the other groups (p less than 0.05). The control group differed from the exercise-trained and shocked group only in diastolic BP (p less than 0.05). During a short-term stress session plasma norepinephrine levels in the exercise-trained and shocked group were significantly lower than those in the shock only group (555 +/- 56 vs 776 +/- 84 pg/ml; p less than 0.05). These results indicate that an alteration of autonomic function resulted from the exercise training, but its contribution to the resistance of the exercise-trained and shocked rats to stress-induced hypertension is unclear.

Analysis of Variance↗