scholarly journals Paraventricular nucleus control of blood pressure in two-kidney, one-clip rats: effects of exercise training and resting blood pressure

2013 ◽  
Vol 305 (11) ◽  
pp. R1390-R1400 ◽  
Author(s):  
Noreen F. Rossi ◽  
Haiping Chen ◽  
Maria Maliszewska-Scislo
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Exercise Training ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Sham Group ◽  
Wheel Running ◽  
Ang Ii ◽  
Nitric Oxide Signaling

Exercise-induced changes in γ-aminobutyric acid (GABA) or nitric oxide signaling within the paraventricular nucleus (PVN) have not been studied in renovascular hypertension. We tested whether exercise training decreases mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) in two-kidney, one-clip (2K-1C) hypertensive rats due to enhanced nitric oxide or GABA signaling within PVN. Conscious, unrestrained male Sprague-Dawley rats with either sham (Sham) or right renal artery clipping (2K-1C) were assigned to sedentary (SED) or voluntary wheel running (ExT) for 6 or 12 wk. MAP and angiotensin II (ANG II) were elevated in 2K-1C SED rats. The 2K-1C ExT rats displayed lower MAP at 6 wk that did not decline further by 12 wk. Plasma ANG II was lower in 2K-1C ExT rats. Increases in MAP, heart rate, and RSNA to blockade of PVN nitric oxide in 2K-1C SED rats were attenuated compared with either Sham group. Exercise training restored the responses in 2K-1C ExT rats. The increase in MAP in response to bicuculline was inversely correlated with baseline MAP. The rise in MAP was lower in 2K-1C SED vs. either Sham group and was normalized in the 2K-1C ExT rats. Paradoxically, heart rate and RSNA responses were not diminished in 2K-1C SED rats but were significantly lower in the 2K-1C ExT rats. Thus the decrease in arterial pressure in 2K-1C hypertension associated with exercise training is likely due to diminished excitatory inputs to PVN because of lower ANG II and higher nitritergic tone rather than enhanced GABA inhibition of sympathetic output.

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

1995 ◽  
Vol 268 (6) ◽  
pp. H2302-H2310 ◽  
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.

scholarly journals Reduced GABA inhibition of sympathetic function in renal-wrapped hypertensive rats

1998 ◽  
Vol 275 (5) ◽  
pp. R1523-R1529 ◽  
Author(s):  
Douglas S. Martin ◽  
Joseph R. Haywood
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Hypertensive Rats ◽  
Sympathetic Function ◽  
Arterial Pressure Measurement ◽  
Gaba Function

Animals with bilateral cannulas in the paraventricular nucleus were made hypertensive by a one-kidney, figure eight renal wrap procedure or sham operated. Femoral artery and vein catheters were inserted for arterial pressure measurement and plasma catecholamine determination. After recovery and 4 days after hypertension surgery, bicuculline methiodide or muscimol was microinjected into the paraventricular nucleus. In some rats, nitroprusside was infused intravenously to reflexly stimulate the sympathetic nervous system. In control rats, bicuculline increased blood pressure, heart rate, and plasma norepinephrine and epinephrine concentrations. In contrast, in hypertensive rats blood pressure did not change while the heart rate response was maintained. Plasma norepinephrine and epinephrine responses were reduced 75 and 68%, respectively. Muscimol injections decreased arterial pressure in the hypertensive rats. Heart rate responses to nitroprusside were similar in the two groups of rats, while the plasma catecholamine responses were attenuated in the hypertensive animals. These data suggest that GABA function in the paraventricular nucleus is reduced in renal wrap hypertension.

Hemodynamic and sympathoadrenal responses to mental stress during nitric oxide synthesis inhibition

2004 ◽  
Vol 287 (5) ◽  
pp. H2309-H2315 ◽  
Author(s):  
Madeleine Lindqvist ◽  
Anders Melcher ◽  
Paul Hjemdahl
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Mental Stress ◽  
Stress Test ◽  
Arterial Plasma ◽  
Forearm Vascular Resistance

Cardiovascular and sympathoadrenal responses to a reproducible mental stress test were investigated in eight healthy young men before and during intravenous infusion of the nitric oxide (NO) synthesis inhibitor N-monomethyl-l-arginine (l-NMMA). Before l-NMMA, stress responses included significant increases in heart rate, mean arterial pressure, and cardiac output (CO) and decreases in systemic and forearm vascular resistance. Arterial plasma norepinephrine (NE) increased. At rest after 30 min of infusion of l-NMMA (0.3 mg·kg−1·min−1 iv), mean arterial pressure increased from 98 ± 4 to 108 ± 3 mmHg ( P < 0.001) because of an increase in systemic vascular resistance from 12.9 ± 0.5 to 18.5 ± 0.9 units ( P < 0.001). CO decreased from 7.7 ± 0.4 to 5.9 ± 0.3 l/min ( P < 0.01). Arterial plasma NE decreased from 2.08 ± 0.16 to 1.47 ± 0.14 nmol/l. Repeated mental stress during continued infusion of l-NMMA (0.15 mg·kg−1·min−1) induced qualitatively similar cardiovascular responses, but there was a marked attenuation of the increase in mean arterial blood pressure, resulting in similar “steady-state” blood pressures during mental stress without and with NO blockade. Increases in heart rate and CO were attenuated, but stress-induced decreases in systemic and forearm vascular resistance were essentially unchanged. Arterial plasma NE increased less than during the first stress test. Thus the increased arterial tone at rest during l-NMMA infusion is compensated for by attenuated increases in blood pressure during mental stress, mainly through a markedly attenuated CO response and suppressed sympathetic nerve activity.

Role of the area postrema in angiotensin II modulation of baroreflex control of heart rate in conscious mice

2003 ◽  
Vol 284 (3) ◽  
pp. H1003-H1007 ◽  
Author(s):  
Baojian Xue ◽  
Hope Gole ◽  
Jaya Pamidimukkala ◽  
Meredith Hay
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Area Postrema ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Intravenous Infusions

This study reports the effects of angiotensin II (ANG II), arginine vasopression (AVP), phenylephrine (PE), and sodium nitroprusside (SNP) on baroreflex control of heart rate in the presence and absence of the area postrema (AP) in conscious mice. In intact, sham-lesioned mice, baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of ANG II were significantly less than those observed with similar increases in arterial pressure with PE (slope: −3.0 ± 0.9 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). Baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of AVP were the same as those observed with PE in sham animals (slope: −5.8 ± 0.7 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). After the AP was lesioned, the slope of baroreflex inhibition of heart rate was the same whether pressure was increased with ANG II, AVP, or PE. The slope of the baroreflex-induced increases in heart rate due to decreases in arterial blood pressure with SNP were the same in sham- and AP-lesioned animals. These results indicate that, similar to other species, in mice the ability of ANG II to acutely reset baroreflex control of heart rate is dependent on an intact AP.

Direct and reflexive effects of nitric oxide synthase inhibition on blood pressure

2008 ◽  
Vol 294 (1) ◽  
pp. H190-H197 ◽  
Author(s):  
Jill M. Wecht ◽  
Joseph P. Weir ◽  
David S. Goldstein ◽  
Annmarie Krothe-Petroff ◽  
Ann M. Spungen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Nitric Oxide Synthase ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Control Group ◽  
Plasma Norepinephrine ◽  
Oxide Synthase

Direct effects of vasoactive substances on blood pressure can be examined in individuals with tetraplegia due to disruption of descending spinal pathways to sympathetic preganglionic neurons, as cervical lesions interfere with baroreceptor reflex buffering of sympathetic outflow. In this study, we assessed effects of the nitric oxide synthase inhibitor nitro-l-arginine methyl ester (l-NAME) on mean arterial pressure, heart rate, and plasma norepinephrine concentrations in individuals with tetraplegia vs. effects shown in a neurologically intact control group. Seven individuals with tetraplegia and seven age-matched controls received, on separate visits and in the following order, placebo (30 ml normal saline) and 0.5, 1, 2, and 4 mg/kg l-NAME intravenously over 60 min. Supine hemodynamic data were collected, and blood was sampled at the end of each infusion and at 120, 180, and 240 min thereafter. l-NAME increased mean arterial pressure, and the relative increase was greater in the tetraplegia group than in the control group. Heart rate was reduced after l-NAME administration in both groups. l-NAME decreased plasma norepinephrine in the control group but not in the group with tetraplegia. These findings suggest that reflexive sympathoinhibition normally buffers the pressor response to nitric oxide synthase inhibition, an effect that is not evident in individuals with tetraplegia as a result of decentralized sympathetic vasomotor control.

Angiotensin receptors contribute to blood pressure homeostasis in salt-depleted SHR

2003 ◽  
Vol 284 (1) ◽  
pp. R164-R173 ◽  
Author(s):  
Shigefumi Nakamura ◽  
David B. Averill ◽  
Mark C. Chappell ◽  
Debra I. Diz ◽  
K. Bridget Brosnihan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Angiotensin Receptors ◽  
Receptor Subtypes ◽  
Ang Ii ◽  
Blood Pressure Lowering Effect ◽  
Blood Pressure Elevation ◽  
Spontaneously Hypertensive

This study evaluated the contribution of angiotensin peptides acting at various receptor subtypes to the arterial pressure and heart rate of adult 9-wk-old male conscious salt-depleted spontaneously hypertensive rats (SHR). Plasma ANG II and ANG I in salt-depleted SHR were elevated sevenfold compared with peptide levels measured in sodium-replete SHR, whereas plasma ANG-(1–7) was twofold greater in salt-depleted SHR compared with salt-replete SHR. Losartan (32.5 μmol/kg), PD-123319 (0.12 μmol · kg−1 · min−1), [d-Ala7]ANG-(1–7) (10 and 100 pmol/min), and a polyclonal ANG II antibody (0.08 mg/min) were infused intravenously alone or in combination. Combined blockade of AT2 and AT(1–7) receptors significantly increased the blood pressure of losartan-treated SHR (+15 ± 1 mmHg; P < 0.01); this change did not differ from the blood pressure elevation produced by the sole blockade of AT(1–7) receptors (15 ± 4 mmHg). On the other hand, sole blockade of AT2 receptors in losartan-treated SHR increased mean arterial pressure by 8 ± 1 mmHg ( P < 0.05 vs. 5% dextrose in water as vehicle), and this increase was less than the pressor response produced by blockade of AT(1–7) receptors alone or combined blockade of AT(1–7) and AT2 receptors. The ANG II antibody increased blood pressure to the greatest extent in salt-depleted SHR pretreated with only losartan (+11 ± 2 mmHg) and to the least extent in salt-depleted SHR previously treated with the combination of losartan, PD-123319, and [d-Ala7]ANG-(1–7) (+7 ± 1 mmHg; P < 0.01). Losartan significantly increased heart rate, whereas other combinations of receptor antagonists or the ANG II antibody did not alter heart rate. Our results demonstrate that ANG II and ANG-(1–7) act through non-AT1receptors to oppose the vasoconstrictor actions of ANG II in salt-depleted SHR. Combined blockade of AT2 and AT(1–7) receptors and ANG II neutralization by the ANG II antibody reversed as much as 67% of the blood pressure-lowering effect of losartan.

scholarly journals Role of Mineralocorticoid and Angiotensin Type 1 Receptors in the Paraventricular Nucleus in Angiotensin-Induced Hypertension

2021 ◽  
Vol 12 ◽  
Author(s):  
Sandra L. Burke ◽  
Benjamin Barzel ◽  
Kristy L. Jackson ◽  
Cindy Gueguen ◽  
Morag J. Young ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Paraventricular Nucleus ◽  
Pressure Control ◽  
Treated Group ◽  
Inhibitory Influence ◽  
Ang Ii ◽  
Air Jet

The hypothalamic paraventricular nucleus (PVN) is an important site where an interaction between circulating angiotensin (Ang) and mineralocorticoid receptor (MR) activity may modify sympathetic nerve activity (SNA) to influence long-term elevation of blood pressure. We examined in conscious Ang II-treated rabbits, the effects on blood pressure and tonic and reflex renal SNA (RSNA) of microinjecting into the PVN either RU28318 to block MR, losartan to block Ang (AT1) receptors or muscimol to inhibit GABAA receptor agonist actions. Male rabbits received a moderate dose of Ang II (24 ng/kg/min subcutaneously) for 3 months (n = 13) or sham treatment (n = 13). At 3 months, blood pressure increased by +19% in the Ang II group compared to 10% in the sham (P = 0.022) but RSNA was similar. RU28318 lowered blood pressure in both Ang II and shams but had a greater effect on RSNA and heart rate in the Ang II-treated group (P &lt; 0.05). Losartan also lowered RSNA, while muscimol produced sympatho-excitation in both groups. In Ang II-treated rabbits, RU28318 attenuated the blood pressure increase following chemoreceptor stimulation but did not affect responses to air jet stress. In contrast losartan and muscimol reduced blood pressure and RSNA responses to both hypoxia and air jet. While neither RU28318 nor losartan changed the RSNA baroreflex, RU28318 augmented the range of the heart rate baroreflex by 10% in Ang II-treated rabbits. Muscimol, however, augmented the RSNA baroreflex by 11% in sham animals and none of the treatments altered baroreflex sensitivity. In conclusion, 3 months of moderate Ang II treatment promotes activation of reflex RSNA principally via MR activation in the PVN, rather than via activation of AT1 receptors. However, the onset of hypertension is independent of both. Interestingly, the sympatho-excitatory effects of muscimol in both groups suggest that overall, the PVN regulates a tonic sympatho-inhibitory influence on blood pressure control.

scholarly journals Intermedin in Paraventricular Nucleus Attenuates Sympathetic Activity and Blood Pressure via Nitric Oxide in Hypertensive Rats

Hypertension ◽  
2014 ◽  
Vol 63 (2) ◽  
pp. 330-337 ◽  
Author(s):  
Ye-Bo Zhou ◽  
Hai-Jian Sun ◽  
Dan Chen ◽  
Tong-Yan Liu ◽  
Ying Han ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Sympathetic Activity ◽  
Hypertensive Rats
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