Instrumental Learning of Systolic Blood Pressure Responses by Curarized Rats: Dissociation of Cardiac and Vascular Changes

Author(s):  
Leo V. DiCara
1984 ◽  
Vol 62 (7) ◽  
pp. 846-849 ◽  
Author(s):  
J. N. Sharma ◽  
P. G. Fernandez ◽  
B. K. Kim ◽  
C. R. Triggle

Systolic blood pressure responses to enalapril maleate (MK 421, a new angiotensin converting enzyme inhibitor (CEI)) and hydrochlorothiazide (HTZ) were studied in conscious Dahl salt-sensitive (DS) and salt-resistant (DR) rats maintained on a high salt (8.0% NaCl) and a normal salt (0.4% NaCl) diet. The DS rats were severely hypertensive after 3 weeks on the high salt diet whereas the systolic blood pressure (SBP) of the DR rats were normotensive. Oral treatment with enalapril (15–100 mg∙kg−1∙day−1) and HTZ (60–400 mg∙kg−1∙day−1) caused a significant reduction of SBP in the DS rats with the high salt diet (P < 0.001); however, this was not observed until after 4 weeks of treatment when the dosage was 30 and 150 mg∙kg−1∙day−1, respectively. Furthermore, enalapril therapy alone significantly reduced the SBP of all groups of rats regardless of diet or Dahl strain (P < 0.001), but this was not observed until the end of the 7th week of therapy in DR rats on 8.0% NaCl and the end of the 3rd week of therapy for DR and DS rats on 0.4%) NaCl. These results suggest that enalapril may lower SBP by mechanisms other than those related to an action as a CEI.


1992 ◽  
Vol 17 (2) ◽  
pp. 107-123 ◽  
Author(s):  
Niels Birbaumer ◽  
Thomas Elbert ◽  
Brigitte Rockstroh ◽  
Johannes Kr�mer ◽  
Werner Lutzenberger ◽  
...  

1997 ◽  
Vol 272 (2) ◽  
pp. H648-H656 ◽  
Author(s):  
B. Csiky ◽  
G. Simon

We tested, in the early stage of angiotensin II (ANG II)-induced hypertension, whether sympathectomy prevented the autopotentiation of vasoconstrictor responses by ANG II and, in the chronic, established phase of hypertension, whether the antihypertensive effect of sympathectomy, if any, was related to the prevention of structural vascular changes. Neonatally and sham-sympathectomized male Sprague-Dawley rats received 100 or 200 ng x kg(-1) x min(-1) ANG II intraperitoneally for 7-10 days or 200 ng x kg(-1) x min(-1) ANG II subcutaneously for 4 wk. Sham-treated sympathectomized and sham-sympathectomized rats were controls. Vasoconstrictor responses to ANG II, norepinephrine (NE), arginine vasopressin, and periarterial nerve stimulation were measured in the mesentery of rats, and thereafter, in the chronically treated rats, mesenteric resistance arteries were fixed in situ for morphometric measurements. In ANG II-treated sham-sympathectomized rats: 1) tail systolic blood pressure was unchanged after 7-10 days and increased by 23 mmHg at 4 wk (P < 0.001); 2) vasoconstrictor responses were selectively increased to ANG II (autopotentiation; P = 0.026) and nerve stimulation (P = 0.031) at 7-10 days and nonselectively increased to all stimuli at 4 wk (P < 0.05 to P < 0.01); and 3) after 4 wk, the wall-to-lumen ratio of resistance arteries was increased (P < 0.02). In ANG II-treated sympathectomized rats, there were no changes in systolic blood pressure or vasoconstrictor responses at either 7-10 days or 4 wk, but structural vascular changes developed to the same extent as in sham-sympathectomized ANG II-treated rats. Autopotentiation of vasoconstrictor responses appears to be due to an interaction between ANG II and the sympathetic nervous system, because it is prevented by sympathectomy. The dissociation of function and structure in the chronic stage of ANG II administration to sympathectomized rats suggests that structural vascular changes by themselves are insufficient to cause hypertension, but increased vascular reactivity or vasoconstrictor input is also needed.


2019 ◽  
Vol 317 (2) ◽  
pp. H415-H423 ◽  
Author(s):  
Dennis P. Pollow ◽  
Joshua A. Uhlorn ◽  
Megan A. Sylvester ◽  
Melissa J. Romero-Aleshire ◽  
Jennifer L. Uhrlaub ◽  
...  

Although it is known that the prevalence and severity of hypertension increases in women after menopause, the contribution of T cells to this process has not been explored. Although the immune system is both necessary and required for the development of angiotensin II (ANG II) hypertension in men, we have demonstrated that premenopausal women are protected from T cell-mediated hypertension. The goal of the current study was to test the hypotheses that 1) female protection against T cell-mediated ANG II hypertension is eliminated following progression into menopause and 2) T regulatory cells (Tregs) provide premenopausal protection against ANG II-induced hypertension. Menopause was induced in Rag-1−/− mice (via 4-vinylcyclohexene diepoxide), and all mice received a 14-day ANG II infusion. Donor CD3+ T cells were adoptively transferred 3 wk before ANG II infusion. In the absence of T cells, systolic blood pressure responses to ANG II were similar to those seen in premenopausal mice (Δ12 mmHg). After adoptive transfer of T cells, ANG II significantly increased systolic blood pressure in postmenopausal females (Δ28 mmHg). A significant increase in F4/80 positive renal macrophages, an increase in renal inflammatory gene expression, along with a reduction in renal expression of mannose receptor C-type 1, a marker for M2 macrophages, accompanied the increase in systolic blood pressure (SBP). Flow cytometric analysis identified that Tregs were significantly decreased in the spleen and kidneys of Rag-1−/− menopausal mice versus premenopausal females, following ANG II infusion. In a validation study, an anti-CD25 antibody was used to deplete Tregs in premenopausal mice, which induced a significant increase in SBP. These results demonstrate that premenopausal protection against T cell-mediated ANG II hypertension is eliminated once females enter menopause, suggesting that a change in hormonal status upregulates macrophage-induced proinflammatory and T cell-dependent responses. Furthermore, we are the first to report that the presence of Tregs are required to suppress ANG II hypertension in premenopausal females. NEW & NOTEWORTHY Whether progression into menopause eliminated female protection against T cell-mediated hypertension was examined. Menopausal mice without T cells remained protected against angiotensin II (ANG II) hypertension; however, in the presence of T cells, blood pressure responses to ANG II increased significantly in menopause. Underlying mechanisms examined were anti-inflammatory protection provided by T regulatory cells in premenopausal females and renal inflammatory processes involving macrophage infiltration and cytokine activation.


2019 ◽  
Vol 8 (2) ◽  
pp. 55-63
Author(s):  
Dimkpa Uchechukwu ◽  
Okoye Chinelo Blessing ◽  
Stephen O. Maduka ◽  
Uchefuna Roy Chinweuba ◽  
Njoku-Oji Nancy Njideka ◽  
...  

ABSTRACT Background: We aimed to assess systolic blood pressure (SBP) responses in relation to the cardiorespiratory fitness (CRF) levels of apparently healthy, young Nigerian adults during and after a submaximal-effort exercise test. Methods: One hundred and twelve young adults (62 males and 50 females) participated in the study and were grouped according to their CRF levels—low, moderate, and high. The participants performed submaximal ergometer exercise tests to elicit exercise and postexercise blood pressure responses. Results: Males and females with high CRF indicated significantly (P &lt; 0.05) higher change of exercise SBP at peak exercise (ΔEx·SBPpeak), and post-SBP decline compared with the other CRF groups. In addition, higher (P &lt; 0.05) ΔEx·SBP2min and faster SBP recovery time were observed in the high CRF group compared to low CRF group. Females with high CRF had a significantly (P &lt; 0.05) higher peak oxygen pulse and energy expenditure compared with the lower CRF groups. There was a very low incidence of abnormal SBP responses among the study population. Conclusion: Greater exercise SBP responses, an indication of higher cardiac output due to greater metabolic demand, and faster SBP recovery were observed in participants with a high CRF compared with the other CRF groups. These findings suggest that regular exercise which maintains a higher CRF in young Nigerian adults may be related to a healthy SBP exercise response.


1993 ◽  
Vol 77 (2) ◽  
pp. 555-563 ◽  
Author(s):  
Phyllis K. Stein ◽  
Stephen H. Boutcher

Heart-rate and blood-pressure responses are assumed to reflect the “stressfulness” of cognitive tasks. Cardiovascular responses to speech are often assumed to be negligible. To test these assumptions, 34 middle-aged men (mean age 45.0 ± 6.1) performed three versions of the Stroop color-conflict task, passive responding, push-button, and verbal. Although difficulty of passive responding was rated 11.8 (fairly light), push-button 16.1 (between hard and very hard), and verbal Stroop 14.5 (hard), all were significantly differenr. Analysis of variance showed during tasks heart-rate responses and systolic blood pressure did not differ. Recovery average heart-rare and over-all heart-rate patterns were not different for the difficult tasks but were significantly different from the easy task. Diastolic blood-pressure changes during tasks were more similar for verbal tasks despite the difference in difficulty. Stressor heart-rate and systolic blood-pressure responses did not reflect the difficulty of this stressful task. Verbalization of responses contributed significantly to cardiovascular reactivity.


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