Reflex control of vasopressin during hemorrhage in hypertensive rabbits

Hypertensive (HT) rabbits have impaired reflex control of heart rate and vascular tone, which is, at least in part, related to dysfunctional baroreceptors. We hypothesized that reflex control of vasopressin (AVP) would also be impaired in the HT rabbit. To test this, we compared hemorrhage-induced increases in AVP between conscious normotensive (NT) and HT rabbits. The hemorrhage-induced rise in AVP was found to be significantly (P < 0.05) attenuated in the HT rabbits. We tested a second hypothesis, that the observed impairment was related to arterial baroreceptor function, by hemorrhaging the same rabbits after reversible cardiac denervation. Under these conditions, only the arterial baroreceptors would be expected to contribute to reflex control of AVP. Impairment was still evident after cardiac denervation; that is, the hemorrhage-induced rise in AVP was significantly (P < 0.01) attenuated in the cardiac-denervated HT rabbits compared with NT rabbits. Thus impairment was, at least in part, related to arterial baroreceptors. Previously, we showed in NT rabbits that AVP only contributed to maintenance of arterial pressure (during hemorrhage), after the autonomic nervous system (ANS) had been blocked. Thus, in the present study, we compared the maintenance of arterial pressure during hemorrhage between NT and HT rabbits after ANS blockade. Blood pressure maintenance was significantly attenuated in the HT rabbits (P < 0.05). In addition, for a given fall in pressure, significantly less AVP (P < 0.05) was released in the ANS-blocked HT rabbits as compared with NT rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Download Full-text

Control of blood pressure and hindlimb conductance during hemorrhage in conscious renal hypertensive rabbits

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.268.6.h2302 ◽

1995 ◽

Vol 268 (6) ◽

pp. H2302-H2310 ◽

Cited By ~ 1

Author(s):

G. Weichert ◽

C. A. Courneya

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Nervous System ◽

Autonomic Nervous System ◽

Angiotensin Ii ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Similar Pattern ◽

Ang Ii ◽

Autonomic Nervous

We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.

Download Full-text

Abstract MP40: Hiv Impairs Endothelial Function And Elevates Blood Pressure Via Tnfa Dependent Mechanisms In Male And Female Mice.

Hypertension ◽

10.1161/hyp.76.suppl_1.mp40 ◽

2020 ◽

Vol 76 (Suppl_1) ◽

Author(s):

Taylor Kress ◽

Eric J Belin De Chantemele ◽

Jessica L Faulkner ◽

Thiago Bruder do Nascimento

Keyword(s):

Blood Pressure ◽

Cardiovascular Disease ◽

Heart Rate ◽

Nervous System ◽

Autonomic Nervous System ◽

Mean Arterial Pressure ◽

Endothelial Dysfunction ◽

Arterial Pressure ◽

Endothelial Function ◽

Viral Infection

HIV is a major health concern with over 37 million individuals worldwide living with HIV. The onset of combination antiretroviral therapy (cART) patients with HIV (PWH) live longer but exhibit accelerated development of cardiovascular disease. Clinical evidence indicates that 35% of PWH exhibit hypertension, however, the etiopathology is still ill-defined. We plan to take advantage of a transgenic mouse model (Tg26) that mimics patients with a repressed virus, to test the hypothesis that viral infection independent of cART induces endothelial dysfunction and hypertension via a TNF-α mediated mechanism. Vascular reactivity was analyzed via wire myography and blood pressure (BP) recorded via radio-telemetry. Results showed that viral infection impaired aorta endothelium-dependent relaxation as reflected by a decrease in acetylcholine-mediated relaxation in both Tg26 mice (P<0.05) which was ameliorated with the NOX 1/4 inhibitor GKT 137831. Smooth muscle cell-dependent relaxation (SNP) and contractility to phenylephrine and KCl remained intact in Tg26 mice. Viral infection increased systolic, diastolic, and mean arterial pressure (MAP: male: WT=112.3±1.3 vs Tg26=121.9±4.0 mmHg/ female: WT=110.6±3.01/ Tg26=120.3±6.9 mmHg) and elevated heart rate (HR) in both sexes (p<0.05). We used atropine, propranolol, and hexamethonium in WT and Tg26 mice to investigate the contribution of the autonomic nervous system to hypertension. HR responses to both atropine (Female: +5.07±2.8% vs. male +4.3±5.4% of baseline) and propranolol (Female: 19.9±6.1% vs. male 12.0±4.3%) revealed no significance or sex differences in WT mice and no effects of viral infection on autonomic control of heart rate in Tg26 mice. BP responses to hexamethonium revealed no effect of sex or viral infection, supporting a limited contribution of the autonomic nervous system to hypertension in Tg26 mice. However, we found that TNFα inhibition with etanercept reduced mean arterial pressure in Tg26 mice to the level of the WT mice (WT=112.3±1.3, Treated=110.1±0.185) and improved endothelial function. These data indicate that HIV infection contributes to cardiovascular disease via inducing endothelial dysfunction and hypertension via NOX and TNFα-dependent mechanisms respectively.

Download Full-text

Autonomic modulation of heart rate and blood pressure in hypertensive subjects with symptoms of anxiety

Clinical Science ◽

10.1042/cs0950043 ◽

1998 ◽

Vol 95 (1) ◽

pp. 43-52 ◽

Cited By ~ 9

Author(s):

Gianfranco PICCIRILLO ◽

Santagada ELVIRA ◽

Emanuela VIOLA ◽

Carmela BUCCA ◽

Michele DURANTE ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Nervous System ◽

Autonomic Nervous System ◽

Arterial Pressure ◽

Left Ventricular ◽

Cardiovascular Control ◽

Anxiety Symptoms ◽

Autonomic Nervous ◽

Sympathetic Modulation

1.The influence of anxiety symptoms on autonomic nervous system cardiovascular control has never been studied in hypertensive subjects. This study was designed to verify the presence of sympathetic hyperactivity in hypertension associated with anxiety symptoms. 2.Neuroautonomic cardiovascular control was evaluated using short-time power spectral analysis of RR and arterial pressure variability at baseline and after the head-up tilt test. The two spectral components principally influenced by the autonomic nervous system are the low-frequency (LF) component, mainly though not exclusively due to sympathetic modulation, and the high-frequency (HF) component, due to parasympathetic activity. The ratio of LF to HF powers (LF:HF) provides an index of the sympathovagal sinus balance. 3.We studied 33 hypertensive subjects (mean age 47±1 years; M:F = 19:14) and 37 normotensive control subjects (mean age: 47±2 years; M:F = 20:17) divided into four subgroups: hypertensive subjects who scored 2 or more on a 5-item anxiety symptom scale, hypertensive subjects who scored 0, normotensive controls who scored 2 or more and normotensive controls who scored 0. LF:HF and LF during rest were significantly higher (P< 0.05) in hypertensive and normotensive groups with an anxiety score of 2 or more compared with the two groups who scored 0. HF of systolic blood pressure was significantly lower in the hypertensive group who scored 2 or more than in the hypertensive group who scored 0 (P< 0.05). Tilt in both hypertensive groups reporting anxiety symptoms left the indexes of sympathetic modulation unchanged. Tilt in hypertensive subjects reporting anxiety symptoms also induced a significant fall in arterial pressure (P< 0.05). The mean left ventricular mass index was significantly higher in the hypertensive subjects who had anxiety scores of 2 or more than in those scoring 0 (144.7±3.0 versus 133.4±2.31, P< 0.05). 4.In conclusion, normotensive and hypertensive subjects reporting anxiety symptoms showed increased sympathetic modulation of heart rate at rest. Higher anxiety scores seem to be associated with the development of left ventricular hypertrophy.

Download Full-text

Autonomic nervous system function in type 2 diabetes using conventional clinical autonomic tests, heart rate and blood pressure variability measures

Indian Journal of Endocrinology and Metabolism ◽

10.4103/2230-8210.83406 ◽

2011 ◽

Vol 15 (3) ◽

pp. 198 ◽

Cited By ~ 11

Author(s):

S Sucharita ◽

Jyothi Idiculla ◽

Mario Vaz ◽

Ganapathi Bantwal ◽

Vageesh Ayyar

Keyword(s):

Blood Pressure ◽

Type 2 Diabetes ◽

Heart Rate ◽

Nervous System ◽

Autonomic Nervous System ◽

Blood Pressure Variability ◽

System Function ◽

Autonomic Tests ◽

Nervous System Function

Download Full-text

Heart Rate and Blood Pressure Changes During Autonomic Nervous System Challenge in Panic Disorder Patients

Psychosomatic Medicine ◽

10.1097/psy.0b013e3181d972c2 ◽

2010 ◽

Vol 72 (5) ◽

pp. 442-449 ◽

Cited By ~ 29

Author(s):

Jose M. Martinez ◽

Amir Garakani ◽

Horacio Kaufmann ◽

Cindy J. Aaronson ◽

Jack M. Gorman

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Nervous System ◽

Autonomic Nervous System ◽

Panic Disorder ◽

Autonomic Nervous ◽

Pressure Changes

Download Full-text

Man, Machine, and Homeostasis

Just Enough Physiology ◽

10.1093/med/9780199797790.003.0018 ◽

2011 ◽

pp. 141-148

Author(s):

James R. Munis

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Nervous System ◽

Autonomic Nervous System ◽

Fundamental Principle ◽

The Body ◽

Set Point ◽

Autonomic Nervous ◽

Claude Bernard ◽

Shed Light

Physiologist Claude Bernard lived in a time when very little was known about the mechanisms underlying physiologic findings, and he had ample access to clues garnered from observing machines. Let's consider homeostasis (a concept championed by Bernard), an example for which an engineered machine shed light on a fundamental principle of physiology. Homeostasis is simply the tendency of the body to maintain important physiologic variables (eg, heart rate, blood pressure, PACO2) at constant, preset values. An example is a simplified mechanical governor that could be used to regulate the rotational speed of a steam engine shaft. ‘Autoregulate’ might be a more apt word because the governor performs without external help or guidance, provided it is designed and built properly. It doesn't take much imagination to see an analogy between the mechanical governor and the autonomic nervous system. Both maintain specific variables at a constant set point through a process of feedback loops.

Download Full-text

Paraventricular stimulation with glutamate elicits bradycardia and pituitary responses

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1989.256.1.r112 ◽

1989 ◽

Vol 256 (1) ◽

pp. R112-R119 ◽

Cited By ~ 14

Author(s):

D. N. Darlington ◽

M. Miyamoto ◽

L. C. Keil ◽

M. F. Dallman

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Nervous System ◽

Autonomic Nervous System ◽

Arterial Blood Pressure ◽

Excitatory Neurotransmitter ◽

Autonomic Nervous ◽

Arterial Blood ◽

Paraventricular Nuclei ◽

Measured Activation

The excitatory neurotransmitter, L-glutamate (0.5 M, pH 7.4), or the organic acid, acetate (0.5 M, pH 7.4), was microinjected (50 nl over 2 min) directly into the paraventricular nuclei (PVN) of pentobarbital sodium-anesthetized rats while arterial blood pressure and heart rate and plasma adrenocorticotropic hormone (ACTH), vasopressin, and oxytocin were measured. Activation of PVN neurons with L-glutamate led to increases in plasma ACTH, vasopressin, and oxytocin and a profound bradycardia (approximately 80 beats/min) with little change in arterial blood pressure. Microinjection of acetate had no effect on the above variables. The decrease in heart rate was shown to be dependent on the concentration of glutamate injected and the volume of injectate. The bradycardia was mediated through the autonomic nervous system because ganglionic blockade (pentolinium tartrate) eliminated the response; atropine and propranolol severely attenuated the bradycardia. The bradycardia was greatest when L-glutamate was microinjected into the caudal PVN. Injections into the rostral PVN or into nuclei surrounding the PVN led to small or nonsignificant decreases in heart rate. Focal electric stimulation (2-50 microA) of the PVN also led to decreases in heart rate and arterial blood pressure. These data suggest that activation of PVN neurons leads to the release of ACTH, vasopressin, and oxytocin from the pituitary and a bradycardia that is mediated by the autonomic nervous system.

Download Full-text