PubMed Health⌕ Search

Biomedical subjects

J E Lawler

Publications and source records attributed to J E Lawler.

13 recordsLinked to original sources
PubMed1992

The borderline hypertensive rat (BHR) as a model for environmentally-induced hypertension: a review and update.

In recent years, the burgeoning disciplines of health psychology and behavioral medicine have renewed interest in the important role that environmental factors can play in the disease process. Nowhere is this concern more well-founded than in the area of cardiovascular disorders, particularly hypertension. Epidemiologists and clinicians have long suspected that stressful life events can be a sufficient trigger for the expression of hypertension in some individuals. To understand better the ways in which these variables interact in the disease process, researchers have tried, with limited success, to produce experimental hypertension in animals by exposing them to stressful environmental paradigms. Additionally, recent investigations using the borderline hypertensive rat (BHR) have demonstrated the important role genetic factors can play in mediating both the behavioral and cardiovascular responses to environmental stressors. The current paper will review these attempts and discuss recent data from experiments using a relatively new animal model that appears to be especially appropriate for the study of environmental-genetic factors in the elaboration of essential hypertension. We will also discuss potential mechanisms by which environmental stress influences arterial pressure and suggest avenues for further inquiry into the stress-disease relationship.

Animals↗
PubMed1991

Family history of hypertension, gender, and cardiovascular responsivity during stress.

The relationships of family history of hypertension and gender to cardiovascular responses to stress were investigated in this research. One hundred twenty-three subjects were monitored while they rested and performed two tasks, reaction time and Ravens progressive matrices. Positive-family history males exhibited higher levels of systolic blood pressure than the negative male group and higher levels of rate pressure product than the positive-family history female group. Positive-family history males also had heart rate levels as high as the females. Female subjects did not differ from each other based on family history. In addition, subjects were grouped by gender and by high- or low-heart rate reactivity. The results suggest that heart rate reactivity has equally broad effects on cardiovascular function for males and females; for males, this reactivity during rests and tasks also tends to be associated with family history of hypertension.

Adolescent↗
PubMed1991

Baroreflex function in chronically stressed borderline hypertensive rats.

A number of previous studies have demonstrated that some aspect of baroreflex function is altered as hypertension develops. However, no studies have determined whether a chronic stressor can alter baroreflex function in the resting state. In the present study, male borderline hypertensive rats (BHR) were divided into three groups: control, stressed daily for 5 weeks, and stressed daily for 11 weeks. At the appropriate time, 7 different dosages of angiotensin II (AII) were given intravenously as a bolus injection. Heart rate (interbeat interval, or IBI) and mean arterial pressure were tracked for 90 subsequent beats. For each group, intercorrelations between pressure and IBI were obtained. In addition, overall means of pressure and IBI for each dosage were computed for each group and plotted. Higher dosages of AII were required to produce a significant correlation between pressure and IBI in the 5-week group compared to control. In the 11-week group, only the highest dosage yielded a significant correlation between pressure and IBI. When data were expressed in terms of the highest pressure and its corresponding IBI for each group, the 5-week-stress group had a shift in set point compared to control. The 11-week group showed a shift in set point and a reduction in gain compared to control animals. The similarity between these findings and those for other models of hypertension is discussed, with special emphasis on the potential role of the central nervous system.

Angiotensin II↗
PubMed1989

Norepinephrine content of discrete brain nuclei in acutely and chronically stressed borderline hypertensive rats.

Forty-three male borderline hypertensive rats were subjected to either 3 days, or 4, 10, or 16 weeks of daily stress. An additional 43 animals served as unstressed, age-matched controls. At the end of study, animals were sacrificed, brains were removed, and cardiovascularly-important nuclei in the brainstem and hypothalamus were removed by micropunch. Assays revealed that norepinephrine (NE) levels were initially elevated in the brainstem in animals stressed for 3 days. As stress continued, NE levels were significantly lower in the brainstem, and eventually in the hypothalamus, of stressed animals. The relationship of these observations to environmentally-induced hypertension is discussed.

Animals↗
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

Lithium chloride stabilizes systolic blood pressure and increases adrenal catecholamines in the spontaneously hypertensive rat.

The effects of daily, intraperitoneal injections of LiCl (3 mEq/kg) on systolic blood pressure (SBP) and adrenal catecholamine levels were measured in spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto rats (WKY). Control animals from each strain were injected with equivalent volumes (0.1 ml/100 g b.wt.) of 0.9% saline (0.15 mEq/kg). SBP in LiCl-treated SHR was significantly lower (p less than 0.05) than that of saline-treated SHR (177 +/- 7 vs. 196 +/- 4 mm Hg, respectively) after one week. After two weeks SBP was lower in LiCl SHR than in saline controls, but this difference was not significant. While SBP of both LiCl and saline treated WKY was not significantly different (146 +/- 4 vs. 147 +/- 8 mm Hg, respectively), SBP in both WKY groups remained lower than the SBP for either group of SHR. LiCl induced a significant weight loss in the SHR, but not in the WKY. Adrenal norepinephrine and epinephrine were significantly (p less than 0.05) higher in LiCl-treated rats of both strains; dopamine was also higher in LiCl-treated rats of both strains, but significant only between SHR-LiCl and SHR controls. It appears that LiCl's effect in slowing the development of hypertension is independent of its action on adrenal catecholamines. The SHR's increased sensitivity to LiCl, relative to weight loss and SBP, may reflect differences in genetic or physiological status of the animal compared to WKY. These differences may be associated with alterations in membrane ion transport systems.

Adrenal Medulla↗
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↗
PubMed1976

Ventricular electrical instability in the conscious dog: effects of psychologic stress and beta adrenergic blockade.

The effect of psychologic stress on cardiac vulnerability was examined in 10 conscious dogs. The repetitive extrasystole threshold was employed as a measure of susceptibility to ventricular fibrillation. Instrumental aversive conditioning constituted a stressful environment. The repetitive extrasystole threshold decreased by nearly 50 percent during 3 days in which the animals were exposed to the stressful environment. When Tolamolol hydrochloride, a cardioselective beta adrenoceptor blocking agent, was administered before a stress session, the repetitive extrasystole threshold was unaltered from the control value. Thus, stress-evoked changes in cardiac vulnerability are mediated through the sympathetic nervous system.

Action Potentials↗