Role of paraventricular nucleus in the cardiogenic sympathetic reflex in rats

2005 ◽  
Vol 288 (2) ◽  
pp. R420-R426 ◽  
Author(s):  
Matthew R. Zahner ◽  
Hui-Lin Pan
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Reflex Response ◽  
Renal Sympathetic Nerve Activity ◽  
Basal Blood Pressure ◽  
Blood Pressure Responses ◽  
Spinal Afferents

Myocardial ischemia stimulates cardiac spinal afferents to initiate a sympathoexcitatory reflex. However, the pathways responsible for generation of increased sympathetic outflow in this reflex are not fully known. In this study, we determined the role of the paraventricular nucleus (PVN) in the cardiogenic sympathetic reflex. Renal sympathetic nerve activity (RSNA) and blood pressure were recorded in anesthetized rats during epicardial application of 10 μg/ml bradykinin. Bilateral microinjection of muscimol (0.5 nmol), a GABAA receptor agonist, was performed to inhibit the PVN. In 10 vehicle-injected rats, epicardial bradykinin significantly increased RSNA 178.4 ± 48.5% from baseline, and mean arterial pressure from 76.9 ± 2.0 to 102.3 ± 3.3 mmHg. Microinjection of muscimol into the PVN significantly reduced the basal blood pressure and RSNA ( n = 12). After muscimol injection, the bradykinin-induced increases in RSNA (111.6 ± 35.9% from baseline) and mean arterial pressure (61.2 ± 1.3 to 74.5 ± 2.7 mmHg) were significantly reduced compared with control responses. The response remained attenuated even when the basal blood pressure was restored to the control. In a separate group of rats ( n = 9), bilateral microinjection of the ionotropic glutamate antagonist kynurenic acid (4.82 or 48.2 nmol in 50 nl) had no significant effect on the RSNA and blood pressure responses to bradykinin compared with controls. These results suggest that the tonic PVN activity is important for the full manifestation of the cardiogenic sympathoexcitatory response. However, ionotropic glutamate receptors in the PVN are not directly involved in this reflex response.

Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

Brain angiotensin II tonically modulates sympathetic baroreflex in rabbit ventrolateral medulla

1996 ◽  
Vol 271 (3) ◽  
pp. H1015-H1021 ◽  
Author(s):  
T. Saigusa ◽  
M. Iriki ◽  
J. Arita
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Inhibitory Effect ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
Renal Sympathetic

The role of endogenous angiotensin II (ANG II) at the level of the rostral (RVLM) and caudal ventrolateral medulla (CVLM) in the control of sympathetic baroreflex function was investigated in urethan-anesthetized rabbits. The baroreflex relationship between mean arterial pressure and integrated renal sympathetic nerve activity (RSNA) was compared before and during microinfusion of saralasin, an ANG II receptor antagonist into RVLM or CVLM. The infusion of saralasin (20 pmol/min) into RVLM reduced the upper plateau, the range, and the range-dependent gain of the baroreflex, as well as the resting level of RSNA. The infusion of saralasin into CVLM augmented the upper plateau, the reflex range, and the range-dependent gain, whereas it did not alter the resting level of RSNA or mean arterial pressure. These results suggest that 1) the ANG II networks in RVLM are tonically active, influencing the resting level of the sympathetic outflow and facilitating the sympathetic baroreflex function, and 2) the ANG II networks in CVLM do not significantly influence the sympathetic activity in the resting state but exert an inhibitory effect on the baroreflex response when arterial pressure falls below the resting level.

scholarly journals Angiotensin responsiveness in hyperfiltering and nonhyperfiltering diabetic rats.

1993 ◽  
Vol 4 (6) ◽  
pp. 1346-1353
Author(s):  
B M Wilkes ◽  
P F Mento ◽  
M A Vernace
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Urine Volume ◽  
Diabetic Rats ◽  
Filtration Fraction ◽  
Blood Pressure Responses ◽  
Systemic Responses ◽  
Normal Controls

Renal and systemic responses to angiotensin II were studied in hyperglycemic diabetic rats (streptozotocin, 60 mg/kg, i.v.) and vehicle-injected controls at 24 h, 1 wk, 2 mo, or at 6 to 12 mo. In normal rats, the GFR was less than 0.80 mL/min per 100 g body wt (0.57 +/- 0.02 mL/min per 100 g body wt; range: 0.40 to 0.79 mL/min per 100 g body wt; N = 45). Hyperfiltration (GFR > or = 0.80 mL/min per 100 g body wt) was observed in all diabetic rats studied at 1 wk (GFR, 1.03 +/- 0.07 mL/min per 100 g body wt; N = 5; P < 0.001 versus control). However, at earlier and later times, GFR was elevated in only 8 of 18 of the diabetic rats (44%), with an overall prevalence of 56% (13 of 23). Mean arterial pressure, plasma glucose, urine volume, and filtration fraction were not different in hyperfiltering diabetic rats compared with nonhyperfiltering diabetic rats or normal controls. Angiotensin II (12.5 ng/kg per minute i.v.) had no effect on GFR in normal rats or nonhyperfiltering diabetic rats, but it normalized GFR in hyperfiltering diabetic rats (0.74 +/- 0.05 mL/min per 100 g body wt). In contrast with the renal effects of angiotensin II, blood pressure responses were similar in hyperfiltering and nonhyperfiltering diabetic rats. The findings that angiotensin II infusion caused a greater fall in GFR in hyperfiltering diabetic rats than in nonhyperfiltering diabetic rats, but that blood pressure responses were similar, suggests a localized abnormality in angiotensin responsiveness in the kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Systemic administration of choline acetyltransferase decreases blood pressure in murine hypertension

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Andrew Stiegler ◽  
Jian-Hua Li ◽  
Vivek Shah ◽  
Tea Tsaava ◽  
Aisling Tynan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Choline Acetyltransferase ◽  
Cell Subset ◽  
Response Duration ◽  
Reduce Blood Pressure ◽  
Genetic Ablation

AbstractAcetylcholine (ACh) decreases blood pressure by stimulating endothelium nitric oxide-dependent vasodilation in resistance arterioles. Normal plasma contains choline acetyltransferase (ChAT) and its biosynthetic product ACh at appreciable concentrations to potentially act upon the endothelium to affect blood pressure. Recently we discovered a T-cell subset expressing ChAT (TChAT), whereby genetic ablation of ChAT in these cells produces hypertension, indicating that production of ACh by TChAT regulates blood pressure. Accordingly, we reasoned that increasing systemic ChAT concentrations might induce vasodilation and reduce blood pressure. To evaluate this possibility, recombinant ChAT was administered intraperitoneally to mice having angiotensin II-induced hypertension. This intervention significantly and dose-dependently decreased mean arterial pressure. ChAT-mediated attenuation of blood pressure was reversed by administration of the nitric oxide synthesis blocker l-nitro arginine methyl ester, indicating ChAT administration decreases blood pressure by stimulating nitic oxide dependent vasodilation, consistent with an effect of ACh on the endothelium. To prolong the half life of circulating ChAT, the molecule was modified by covalently attaching repeating units of polyethylene glycol (PEG), resulting in enzymatically active PEG-ChAT. Administration of PEG-ChAT to hypertensive mice decreased mean arterial pressure with a longer response duration when compared to ChAT. Together these findings suggest further studies are warranted on the role of ChAT in hypertension.

Sympathetic and blood pressure responses to voluntary apnea are augmented by hypoxemia

1994 ◽  
Vol 77 (5) ◽  
pp. 2360-2365 ◽  
Author(s):  
J. C. Hardy ◽  
K. Gray ◽  
S. Whisler ◽  
U. Leuenberger
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Sleep Apnea Syndrome ◽  
Transient Pressure ◽  
Air Exposure ◽  
Healthy Humans ◽  
Blood Pressure Responses ◽  
Voluntary Apnea

Oscillations of arterial pressure during sleep are the hemodynamic hallmark of the sleep apnea syndrome. The mechanism of these transient pressure elevations is incompletely understood. To investigate the role of the arterial chemoreflex in the neurocirculatory responses to apnea, we measured mean arterial pressure (MAP; Finapres) and muscle sympathetic nerve activity (MSNA; peroneal microneurography) during voluntary end-expiratory apnea during exposure to room air, 10.5% O2 in N2 (hypoxemia), and 100% O2 (hyperoxia) in 11 healthy men. While the men breathed spontaneously, MSNA (in bursts/min) rose during hypoxemia and decreased during hyperoxia and MAP remained unchanged. During room air exposure, apnea led to a rise of 94 +/- 54% in MSNA total amplitude and a rise of 6.5 +/- 2.1 mmHg in MAP. MSNA and MAP increased by 616 +/- 158% and 10.8 +/- 2.4 mmHg, respectively, during hypoxemic apnea of equal duration (time-matched responses) and by 98 +/- 41% and 4.9 +/- 2.0 mmHg, respectively, during hyperoxic apnea (P < 0.05 for hypoxemic vs. hyperoxic apnea for both). Thus, in awake healthy humans, activation of the arterial chemoreflex by hypoxemia appears to contribute importantly to the sympathetic and blood pressure responses to apnea.

scholarly journals Hemodynamic defense response to thyrotropin-releasing hormone injected into medial preoptic nucleus in rats

1991 ◽  
Vol 261 (2) ◽  
pp. R305-R312 ◽  
Author(s):  
A. L. Siren ◽  
S. Vonhof ◽  
G. Feuerstein
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Defense Response ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

The role of thyrotropin-releasing hormone (TRH) and glutamate in central cardiovascular control was studied by microinjections (50 nl) of these agents into the medial or median preoptic nuclei of conscious rats (n = 49) with continuous recording of mean arterial pressure, heart rate, blood flow, and vascular resistance in hindquarter, renal, and mesenteric blood vessels. In addition, the effect of TRH on renal sympathetic nerve activity was studied in anesthetized rats. TRH (2.4-240 pmol) elicited the typical hemodynamic pattern of the "defense response" consisting of increased blood pressure, tachycardia, hindquarter vasodilation, and constriction of renal and mesenteric blood vessels. Maximum changes in cardiovascular variables after the 24-pmol dose were +12 +/- 2 mmHg (mean arterial pressure), +73 +/- 15 beats/min (heart rate), -21 +/- 6% (hindquarter resistance), +15 +/- 6% (renal resistance), and +31 +/- 6% (mesenteric resistance), P less than 0.05 compared with saline. In anesthetized rats, TRH at the 2.4-pmol dose increased renal sympathetic nerve activity (greater than 200%, n = 5, P less than 0.05 compared with control) with no effect on blood pressure or renal flow. Glutamate (10 or 100 nmol) produced a similar pattern of hemodynamic changes as TRH. Peak effects after the 100-nmol dose of glutamate were +16 +/- 2 mmHg (mean arterial pressure), +57 +/- 11 beats/min (heart rate), -31 +/- 3% (hindquarter resistance), +29 +/- 9% (renal resistance), and +87 +/- 22% (mesenteric resistance), P less than 0.05 compared with saline. The glutamate N-methyl-D-aspartate (NMDA) receptor blocker MK-801 (300 micrograms/kg iv) attenuated the pressor-tachycardic responses to TRH and the pressor-mesenteric constrictor responses to glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased blood pressure responses in neuropeptide Y transgenic rats

2001 ◽  
Vol 281 (2) ◽  
pp. R417-R426 ◽  
Author(s):  
Mieczyslaw Michalkiewicz ◽  
Teresa Michalkiewicz ◽  
David L. Kreulen ◽  
Stuart J. McDougall
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Neuropeptide Y ◽  
Sympathetic Nerves ◽  
Sprague Dawley ◽  
Transgenic Rats ◽  
Resting Blood Pressure ◽  
Blood Pressure Responses

Considering the coexistence of neuropeptide Y (NPY) and norepinephrine in perivascular sympathetic nerves and the known vasoconstrictor cooperation of NPY with norepinephrine, we investigated the involvement of NPY in long-term control of cardiovascular functions using NPY transgenic (NPY-tg) rats. These rats were developed by injection of the rat (Sprague-Dawley) pronuclei with a 14.5-kb clone of the rat structural NPY gene. When compared with nontransgenic littermates, NPY concentrations were significantly increased in a number of cardiovascular tissues of NPY-tg hemizygotes. Direct basal mean arterial pressure and heart rate were not changed, but calculated total vascular resistance was significantly increased in NPY-tg subjects. Arterial pressure increases, in response to norepinephrine injection, were greater in the NPY-tg rats. Also, the hypotension and bradycardia in response to hemorrhage were significantly reduced in NPY-tg subjects. These results indicate that NPY, when expressed in increased amounts, potentiates the pressor effects of norepinephrine and contributes to maintaining blood pressure during hemorrhage, but it does not alter resting blood pressure. These transgenic rats will facilitate studies of the role of NPY signaling in cardiovascular regulation, particularly regarding its functional cooperation with norepinephrine.

β-Endorphin, An Endogenous Depressor Agent in the Rat?

1981 ◽  
Vol 61 (s7) ◽  
pp. 339s-342s ◽  
Author(s):  
M. A. Petty ◽  
J. M. A. Sitsen ◽  
W. De Jong
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Subcutaneous Administration ◽  
Nucleus Tractus Solitarii ◽  
Variable Effect ◽  
A Site ◽  
Renal Hypertensive Rats

1. The role of opiates in cardiovascular regulation has been investigated. 2. In urethane-anaesthetized renal hypertensive rats (two-kidney, one-clip Goldblatt model), intracerebroventricular β-endorphin (10 μg) caused a greater fall in mean arterial pressure than in sham-operated controls. 3. Unilateral injection of β-endorphin into the nucleus tractus solitarii of the urethane-anaesthetized rat resulted in a U-shaped dose—response relationship, with a fall in mean arterial pressure and heart rate occurring at low doses. Doses above 10 ng caused a rise in pressure, accompanied by a variable effect on heart rate. 4. The fall in blood pressure and heart rate was prevented by prior subcutaneous administration of naloxone. Naloxone caused an increase in blood pressure when administered alone. 5. These results suggest a depressor role of an endogenous brain opiate, possibly β-endorphin; a site of action is probably the nucleus tractus solitarii.

scholarly journals Brain Testosterone-CYP1B1 (Cytochrome P450 1B1) Generated Metabolite 6β-Hydroxytestosterone Promotes Neurogenic Hypertension and Inflammation

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 1006-1018
Author(s):  
Purnima Singh ◽  
Shubha Ranjan Dutta ◽  
Chi Young Song ◽  
SaeRam Oh ◽  
Frank J. Gonzalez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cytochrome P450 ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Male Mice ◽  
Cytochrome P450 1B1 ◽  
Induced Hypertension ◽  
The Brain

Previously, we showed that peripheral administration of 6β-hydroxytestosterone, a CYP1B1 (cytochrome P450 1B1)-generated metabolite of testosterone, promotes angiotensin II-induced hypertension in male mice. However, the site of action and the underlying mechanism by which 6β-hydroxytestosterone contributes to angiotensin II-induced hypertension is not known. Angiotensin II increases blood pressure by its central action, and CYP1B1 is expressed in the brain. This study was conducted to determine whether testosterone-CYP1B1 generated metabolite 6β-hydroxytestosterone locally in the brain promotes the effect of systemic angiotensin II to produce hypertension in male mice. Central CYP1B1 knockdown in wild-type ( Cyp1b1 +/+ ) mice by intracerebroventricular-adenovirus-GFP (green fluorescence protein)-CYP1B1-short hairpin (sh)RNA attenuated, whereas reconstitution of CYP1B1 by adenovirus-GFP-CYP1B1-DNA in the paraventricular nucleus but not in subfornical organ in Cyp1b1 −/− mice restored angiotensin II-induced increase in systolic blood pressure measured by tail-cuff. Intracerebroventricular-testosterone in orchidectomized (Orchi)- Cyp1b1 +/+ but not in Orchi- Cyp1b1 −/− , and intracerebroventricular-6β-hydroxytestosterone in the Orchi- Cyp1b1 −/− mice restored the angiotensin II-induced: (1) increase in mean arterial pressure measured by radiotelemetry, and autonomic imbalance; (2) reactive oxygen species production in the subfornical organ and paraventricular nucleus; (3) activation of microglia and astrocyte, and neuroinflammation in the paraventricular nucleus. The effect of intracerebroventricular-6β-hydroxytestosterone to restore the angiotensin II-induced increase in mean arterial pressure and autonomic imbalance in Orchi- Cyp1b1 −/− mice was inhibited by intracerebroventricular-small interfering (si)RNA-androgen receptor (AR) and GPRC6A (G protein-coupled receptor C6A). These data suggest that testosterone-CYP1B1-generated metabolite 6β-hydroxytestosterone, most likely in the paraventricular nucleus via AR and GPRC6A, contributes to angiotensin II-induced hypertension and neuroinflammation in male mice.

scholarly journals Blood Pressure Responses in Isokinetic Dynamometry Test in Elderly Community Women: An Exploratory Study

Motricidade ◽  
2018 ◽  
Vol 14 (4) ◽  
pp. 52-56
Author(s):  
Rubens Vinícius Letieri ◽  
Guilherme Eustáquio Furtado ◽  
Taís Rieping ◽  
Mayrhon José Abrantes Farias ◽  
Ana Maria Miranda Botelho Teixeira
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Elderly Women ◽  
Health Hazard ◽  
Age Groups ◽  
Knee Extension ◽  
Isokinetic Test ◽  
Group 2 ◽  
Blood Pressure Responses

The aim of the study was to verify the systolic, diastolic and mean arterial pressure response in elderly women during isokinetic test. The study included 54 females (68.8 ± 5.9 years) divided into two age groups (Group 1: 60 to 70 and group 2: above 71 years). BP was measured before and immediately after the isokinetic knee extension / flexion test in the concentric-concentric mode. After the test, significant elevations were observed in relation to the pre-test in SBP (G1: Δ% = 29.7%, G2: Δ% = 20.6%, p <.01, respectively) and in MAP (G1: Δ% = 7.6 %, G2: Δ% = 8.4%, p <.01, respectively). The use of isokinetic tests produces elevations in systolic blood pressure and mean arterial pressure in elderly women. Increases occur independently of the age group studied. However, the increases detected do not appear to be of sufficient magnitude to constitute a health hazard whereby isokinetic tests can be safely applied in this population.

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