Interactions between ANP and ANG II in regulating blood pressure and sympathetic outflow

1991 ◽  
Vol 260 (6) ◽  
pp. R1145-R1151 ◽  
Author(s):  
M. K. Steele ◽  
D. G. Gardner ◽  
P. L. Xie ◽  
H. D. Schultz
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Contrast Injection ◽  
Synthesis Inhibitor ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Renal Sympathetic

In anesthetized rats with sinoaortic denervation, intracerebroventricular (icv) injection of atrial natriuretic peptide (ANP) resulted in decreased mean arterial blood pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) (depressor effects), whereas icv angiotensin II (ANG II) produced increases in these variables (pressor effects). The depressor effects of ANP were slower in onset and longer in duration than the pressor effects of ANG II. Intracerebroventricular injection of the ANG II-receptor blocker sarthran or the ANG II-synthesis inhibitor captopril resulted in a significant reduction in MAP; HR and RSNA were not affected. Both sarthran and captopril abolished the depressor responses to icv ANP. In contrast, injection of an anti-rat ANP antibody, which blocked the depressor effects of icv ANP, did not by itself modify MAP, HR, or RSNA, nor did the antibody affect the pressor responses to icv ANG II. These data suggest that, in this animal model, the depressor effects of icv ANP are mediated by the inhibition of brain ANG II-dependent neural activity. These results also demonstrate that, in this preparation, the endogenous ANG II system actively contributes to the maintenance of basal MAP, whereas the central ANP system, at least in regions accessible to the antirat ANP antibody, plays little role in this maintenance.

Angiotensin II acutely attenuates range of arterial baroreflex control of renal sympathetic nerve activity

2000 ◽  
Vol 279 (4) ◽  
pp. H1804-H1812 ◽  
Author(s):  
Max G. Sanderford ◽  
Vernon S. Bishop
Keyword(s):  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Renal Sympathetic

Acutely increasing peripheral angiotensin II (ANG II) reduces the maximum renal sympathetic nerve activity (RSNA) observed at low mean arterial blood pressures (MAPs). We postulated that this observation could be explained by the action of ANG II to acutely increase arterial blood pressure or increase circulating arginine vasopressin (AVP). Sustained increases in MAP and increases in circulating AVP have previously been shown to attenuate maximum RSNA at low MAP. In conscious rabbits pretreated with an AVP V1 receptor antagonist, we compared the effect of a 5-min intravenous infusion of ANG II (10 and 20 ng · kg−1 · min−1) on the relationship between MAP and RSNA when the acute pressor action of ANG II was left unopposed with that when the acute pressor action of ANG II was opposed by a simultaneous infusion of sodium nitroprusside (SNP). Intravenous infusion of ANG II resulted in a dose-related attenuation of the maximum RSNA observed at low MAP. When the acute pressor action of ANG II was prevented by SNP, maximum RSNA at low MAP was attenuated, similar to that observed when ANG II acutely increased MAP. In contrast, intravertebral infusion of ANG II attenuated maximum RSNA at low MAP significantly more than when administered intravenously. The results of this study suggest that ANG II may act within the central nervous system to acutely attenuate the maximum RSNA observed at low MAP.

Mechano- and chemoreceptor modulation of renal sympathetic nerve activity at birth in fetal sheep

1999 ◽  
Vol 276 (5) ◽  
pp. R1295-R1301 ◽  
Author(s):  
Jeffrey L. Segar ◽  
Oliva J. Smith ◽  
Aaron T. Holley
Keyword(s):  
Blood Pressure ◽  
Cesarean Section ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Afferent Input ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Physiological responses at birth include increases in heart rate (HR), blood pressure, sympathetic nerve activity, and circulating vasoactive peptides. The factors mediating these responses are not known. To test the hypothesis that afferent input from peripheral mechanoreceptors (arterial and cardiopulmonary baroreceptors) and chemoreceptors contribute to the sympathoexcitatory and hormonal responses at birth, we studied the effects of sinoaortic denervation (SAD) and SAD with vagotomy (Vx) on changes in HR, mean arterial blood pressure (MABP), renal sympathetic nerve activity (RSNA), and catecholamine, arginine vasopressin (AVP), and ANG II levels at birth in term sheep. One hour after delivery by cesarean section, RSNA increased by 168 ± 49 and 192 ± 32% (relative to fetal values) in SAD and SAD-Vx animals, respectively. Significant increases in HR (18 ± 5 and 20 ± 6%) and MABP (24 ± 4 and 20 ± 5%) were also observed 1 h after delivery in SAD and SAD-Vx lambs, respectively. These responses are similar to those seen in intact sheep delivered at the same gestational age. AVP levels markedly increased after birth (19.8 ± 6.7 to 136.1 ± 75.9 pg/ml) in SAD-Vx lambs, whereas SAD animals displayed no change in AVP concentrations. Plasma ANG II also did not change after birth in either group, although levels were consistently higher ( P < 0.01) in SAD compared with SAD-Vx animals. In the presence of SAD, Vx resulted in significantly greater plasma levels of norepinephrine, although levels did not change after birth in either group. The epinephrine responses at birth were similar in both groups of animals. The present data suggest that afferent input from peripheral chemoreceptors and mechanoreceptors contributes little to the hemodynamic and sympathetic responses after delivery by cesarean section. On the other hand, these peripheral mechanisms appear to be involved in modulating endocrine responses at birth.

scholarly journals Renal sympathoinhibition mediated by 5-HT1Areceptors in the RVLM during severe hemorrhage in rats

2002 ◽  
Vol 282 (1) ◽  
pp. R122-R130 ◽  
Author(s):  
C. Dean ◽  
M. Bago
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Severe Hemorrhage ◽  
Renal Sympathetic

The role of 5-hydroxytryptamine type 1A (5-HT1A) receptors in the rostral ventrolateral medulla (RVLM) in the mediation of the sympathoinhibitory and hypotensive responses to severe hemorrhage was examined in pentobarbital sodium-anesthetized rats. The control response to hemorrhage (1 ml/min to 50 mmHg) consisted of a fall in arterial blood pressure and an initial baroreflex increase in renal sympathetic nerve activity followed after 2 min by a rapid decline in blood pressure accompanied by a decrease in renal sympathetic nerve activity. In response to hemorrhage in animals in which the specific 5-HT1A receptor antagonist WAY-100635 was microinjected into the pressor area of the RVLM, the fall in blood pressure was delayed and attenuated while renal sympathetic nerve activity was increased and maintained above baseline. In barodenervated animals with blockade of RVLM 5-HT1A receptors, there was no change in renal sympathetic nerve activity in response to hemorrhage. These data suggest that renal sympathoinhibition elicited in response to severe hemorrhage is mediated by 5-HT1A receptors in the RVLM.

Sympathoinhibition from ventrolateral periaqueductal gray mediated by the caudal midline medulla

2005 ◽  
Vol 289 (5) ◽  
pp. R1477-R1481 ◽  
Author(s):  
C. Dean
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Periaqueductal Gray ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Depressor Response ◽  
Arterial Blood ◽  
Renal Sympathetic

Activation of neurons in the ventrolateral region of the periaqueductal gray (vlPAG) can elicit a decrease in renal sympathetic nerve activity and blood pressure. The present study investigated whether the vlPAG-evoked sympathoinhibitory response depends on neurons in the caudal midline medulla (CMM). In pentobarbital-anesthetized rats, activation of neurons in the vlPAG evoked a decrease in renal sympathetic nerve activity to 29.4 ± 4.8% below baseline levels and arterial blood pressure fell 8.9 ± 1.6 mmHg ( n = 20). Microinjection of the GABA agonist muscimol into sympathoinhibitory regions of the CMM significantly attenuated the vlPAG-evoked sympathoinhibition to 17.9 ± 4.1% below baseline and the depressor response to 4.3 ± 1.2 mmHg. At 65% (13/20) of the sites examined, the vlPAG-evoked sympathoinhibition was responsive to CMM muscimol microinjection and attenuated from 34.2% to 11.5%, with the depressor response reduced from 14.8 to 3 mmHg. Microinjection of muscimol at the remaining 35% of the CMM sympathoinhibitory sites was ineffective on the vlPAG-evoked sympathoinhibition and depressor response. These data indicate that sympathoinhibitory and hypotensive responses elicited by activation of neurons in the vlPAG can be mediated by neurons in the sympathoinhibitory region of the CMM. The finding that the vlPAG-evoked response is not affected by muscimol at all CMM sympathoinhibitory sites also suggests that sympathoinhibitory sites in the CMM are not homogeneous and can mediate functionally different responses.

Acute inhibition of the hypothalamic paraventricular nucleus decreases renal sympathetic nerve activity and arterial blood pressure in water-deprived rats

2004 ◽  
Vol 286 (4) ◽  
pp. R719-R725 ◽  
Author(s):  
Sean D. Stocker ◽  
Kimberly J. Keith ◽  
Glenn M. Toney
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Renal Sympathetic

The present study was performed to determine whether sympathetic outflow and arterial blood pressure in water-deprived rats are dependent on the ongoing neuronal activity of the hypothalamic paraventricular nucleus (PVN). Renal sympathetic nerve activity (RSNA), mean arterial blood pressure (MAP), and heart rate were recorded in urethane-α-chloralose-anesthetized rats that were deprived of water but not food for 48 h before experiments. Acute inhibition of the PVN by bilateral microinjection of the GABAA agonist muscimol (100 pmol/side) significantly decreased RSNA in water-deprived rats (-26.7 ± 4.7%, n = 7) but was without effect in control rats (1.3 ± 6.3%, n = 7). Similarly, injection of muscimol produced a greater decrease in MAP in water-deprived rats than in control rats (-46 ± 3 vs. -16 ± 3 mmHg, respectively), although baseline MAP was not different between groups (105 ± 4 vs. 107 ± 4 mmHg, respectively). Neither bilateral microinjection of isotonic saline vehicle (100 nl/side) into the PVN nor muscimol (100 pmol/side) outside the PVN altered RSNA or MAP in either group. In addition, ganglionic blockade with hexamethonium (30 mg/kg iv) significantly decreased MAP in both groups; however, the decrease in MAP was significantly greater in water-deprived rats than in control rats (62 ± 2 vs. 48 ± 2 mmHg, respectively). Collectively, these findings suggest that sympathetic outflow contributes more to the maintenance of blood pressure in the water-deprived rat, and this depends, at least partly, on the ongoing activity of PVN neurons.

Ontogeny of baroreflex control of renal sympathetic nerve activity and heart rate

1992 ◽  
Vol 263 (6) ◽  
pp. H1819-H1826 ◽  
Author(s):  
J. L. Segar ◽  
G. Hajduczok ◽  
B. A. Smith ◽  
D. C. Merrill ◽  
J. E. Robillard
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Baroreflex Function ◽  
Baroreceptor Stimulation ◽  
Renal Sympathetic

The purpose of this study was to characterize the developmental changes in baroreflex function during fetal and postnatal life in sheep. Resting mean arterial blood pressure increased significantly from 55 +/- 2 mmHg in fetuses to 86 +/- 3 mmHg in newborn lambs and to 105 +/- 4 mmHg in 4- to 6-wk-old lambs. The sensitivity (gain) of the renal sympathetic nerve activity (RSNA) response to baroreceptor stimulation was greater (P < 0.05) in fetuses (-7.7 +/- 1.9%/mmHg) than in newborn (-2.9 +/- 0.1%/mmHg) and 4- to 6-wk-old lambs (-2.2 +/- 0.2%/mmHg). The threshold and saturation pressures for the baroreflex function curve were lower (P < 0.05) in fetuses (44 +/- 2 and 61 +/- 2 mmHg) than in newborn (59 +/- 4 and 106 +/- 5 mmHg) or 4- to 6-wk-old lambs (78 +/- 5 and 132 +/- 6 mmHg). Similar findings were observed when the heart rate response to baroreceptor stimulation was examined. Additional experiments were performed in newborn and 4- to 6-wk-old lambs to determine whether the rise in arterial blood pressure associated with postnatal maturation contributed to baroreflex resetting. Sustained elevation of arterial blood pressure by 15–20 mmHg for over 90 min did not reset the baroreflex function curve in either newborn or 4- to 6-wk-old lambs.(ABSTRACT TRUNCATED AT 250 WORDS)

Are prostaglandins involved in atrial natriuretic peptide mechanisms of cardiovascular control?

1999 ◽  
Vol 77 (3) ◽  
pp. 211-215 ◽  
Author(s):  
Karim S Bandali ◽  
Uwe Ackermann
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Prostaglandin Synthesis ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Renal Sympathetic

Atrial natriuretic peptide (ANP) can excite cardiac nerve endings and invoke a decrease in arterial blood pressure and a reduction in renal sympathetic nerve activity. Our laboratory has previously demonstrated that this renal depressor reflex was invoked by systemic injection of ANP and not by the direct application of ANP to the epicardium, a major locus for vagal afferents. We now examine whether inhibition of prostaglandin synthesis impairs reflex responses that are normally associated with ANP injections. Renal sympathetic nerve activity, arterial blood pressure, and heart rate were recorded in anesthetized rats. Indomethacin was used to inhibit prostaglandin synthesis through the cyclooxygenase pathway. The ANP-mediated decrease in arterial blood pressure and renal sympathetic nerve activity, observed when prostaglandin synthesis was inhibited, did not differ significantly from the decreases observed in these parameters when prostaglandin synthesis was not inhibited. Heart rate remained unchanged. Our results suggest that the sympatho-inhibitory effects of ANP do not require prostaglandins as intermediary compounds.Key words: sympathetic nervous system, renal nerves, prostaglandins.

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