Central cardiovascular effects of AVP and ANP in normotensive and spontaneously hypertensive rats

Stepniakowski, K; Budzikowski, Adam S.; Lon, S.; Szczepañska‐Sadowska, Ewa

doi:10.1016/0165-1838(94)90063-9

Cited by 16 publications

(10 citation statements)

References 39 publications

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“…The specificity of VP microinjection in SFO is further supported by our demonstration that VP microinjection into the third ventricle produced large, long-lasting in creases in BP. The peak increase (approximately 7 mm Hg) in BP observed following administration into the third ventricle is consistent with previous studies showing that ventricular administration (lateral ventricle) of VP causes an increase of 6 mm Hg in BP [3].…”

Section: Discussionsupporting

confidence: 78%

“…Vasopressin (VP), in addition to its important role in the maintenance of cardiovascular function through di rect vasoconstrictor actions, has been repeatedly suggest ed to play significant central roles in the control of blood pressure (BP) [1][2][3]. However, circulating peptides are normally prevented from accessing neural elements with in the central nervous system (CNS) by the blood brain barrier.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Vasopressin Acts in the Subfornical Organ to Decrease Blood Pressure

Smith¹,

Ferguson²

1997

Neuroendocrinology

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In addition to its traditional role as a circulating vasoactive peptide, vasopressin (VP) has been shown to play significant roles in central cardiovascular processing. The recent description of VP receptors within the subfomical organ (SFO) has suggested this circumventricular organ (CVO) as a potential locus for feedback actions of circulating VP on the brain. The well-established anatomical connections between SFO and hypothalamic autonomic control centers provide further arguments in support of such a view. This study was undertaken to determine the physiological consequences of activation of VP receptors within the SFO of urethane anesthetized rats. Micro injection (0.5 µl) of 5 pmol VP into SFO resulted in significant decreases in blood pressure (BP, mean AUC-638.3 ± 110.3 mm Hg·s, p < 0.01, n = 13) without a change in heart rate (HR, mean AUC 7.9 ± 14.0 beats, p > 0.05, n = 12), effects which were repeatable. These depressor effects were specific to microinjection locations within this CVO as similar VP microinjections into non-SFO tissue were without effect on BP (mean AUC 245.4 ± 111.5 mm Hg·s, p > 0.05, n = 10), or HR (mean AUC 1.8 ± 3.1 beats, p > 0.05, n = 9). In contrast to the former depressor effects, VP microinjection (5 pmol in 0.5 µl) into the third ventricle produced large increases in BP (mean AUC 1,461.8 ± 368.97 mm Hg·s, p < 0.05, n = 6) again with no change in HR (mean AUC 1.4 ± 5.96 beats, p > 0.05, n = 6). The hypotensive effects observed in response to VP microinjection into SFO were abolished by systemic treatment with a V₁ receptor antagonist (mean AUC 89.5 ± 67.7 mm Hg·s, p > 0.05) compared to BP response before V₁ receptor blockade (mean AUC -605.9 ± 119.8 mm Hg·s, n = 4). These results suggest that the SFO may be an essential structure in the feedback control loop through which circulating VP influences descending autonomic pathways involved in cardiovascular control.

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Section: Discussionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Vasopressin Acts in the Subfornical Organ to Decrease Blood Pressure

Smith¹,

Ferguson²

1997

Neuroendocrinology

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“…Further, neuronally produced ANP can act directly on neurons in the brain to modify arterial pressure and cardiovascular responses (3)(4)(5). Altered synthesis and/or release of ANP in critical brain nuclei appears to contribute to hypertension in spontaneously hypertensive rats (SHR; 6, 7) and in Dahl-NaCl sensitive rats (8).…”

Section: Introductionmentioning

confidence: 99%

“…A second experiment tested more directly the role of endogenous ANP in this model by infusing into the AHA c-ANP, (ANP [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] ), a peptide fragment of ANP that binds to the ANP clearance receptor (ANP-C) and thereby decreases the ability of the ANP-C receptor to bind to and take up endogenously released ANP. This results in an elevation of extracellular ANP in the AHA.…”

Section: Introductionmentioning

confidence: 99%

Atrial natriuretic peptide regulation of noradrenaline release in the anterior hypothalamic area of spontaneously hypertensive rats.

Peng¹,

Oparil²,

Meng³

et al. 1996

J. Clin. Invest.

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In spontaneously hypertensive rats (SHR), high NaCl diets increase arterial pressure and sympathetic nervous system activity by decreasing noradrenaline release in the anterior hypothalamic area (AHA), thereby reducing the activation of sympathoinhibitory neurons in AHA. Atrial natriuretic peptide (ANP) can inhibit the release of noradrenaline, and ANP concentration is elevated in the AHA of SHR. The present study tests the hypothesis that in SHR, local ANP inhibits noradrenaline release from nerve terminals in AHA. Male SHR fed a basal or high NaCl diet for 2 wk and normotensive Wistar Kyoto rats (WKY) fed a basal NaCl diet were studied. In SHR on the basal diet, microperfusion of exogenous ANP into the AHA elicited a dose-related decrease in the concentration of the major noradrenaline metabolite 3-methoxy-4-hydroxy-phenylglycol (MOPEG) in the AHA; this effect was attenuated in the other two groups.

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“…It is well known that in hypertensive rats, as well as in humans with essential hypertension, there is an increase in the peripheral sympathetic activity that includes reduction in BG, [24][25][26][27][28][29] and maybe FEL has a different interaction with these special patients. However, these authors did not compare the effect of EPI and FEL in these patients, and EPI may be more hazardous than FEL in these situations, because it has a smaller ratio of Ϫ⌬HR to ⌬MAP than FEL.…”

mentioning

confidence: 99%

Cardiovascular Effects of Felypressin

Cecanho

Luca

Ranali

2006

Anesthesia Progress

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and ‡Professor of Dentistry, School of Piracicaba-UNICAMP, Piracicaba, Brazil Cardiovascular effects of felypressin (FEL) were studied in Wistar rats. Heart rate and mean arterial pressure measurements were taken in awake rats treated with vasopressin (AVP), FEL, or epinephrine (EPI). Each group received either an intravenous (IV) or an intracerebroventricular V 1 receptor antagonist, saline, area postrema removal, or sham surgery. Analysis of variance and Student-Newman-Keuls (P Ͻ .05) were applied. Felypressin and AVP induced a pressor effect, and bradycardia was inhibited by IV V 1 antagonist. Intracerebroventricular V 1 antagonist and area postrema removal enhanced their pressor effects. Epinephrine induced a higher pressor effect and a similar bradycardia that was not affected by the treatments. It was concluded that FEL depends on V 1 receptors to induce pressor and bradycardic effects, and that it produces a high relationship between bradycardia and mean arterial pressure variation depending on area postrema and central V 1 receptors. These effects are potentially less harmful to the cardiovascular system than the effects of EPI.Key Words: Anesthesia, local; Vasoconstrictor agents; Blood pressure; Baroreflex; Vasopressin. F elypressin (FEL), a synthetic analogue of vasopressin (AVP), has been widely used as a substitute for epinephrine (EPI) in anesthetic solutions to promote local vasoconstriction during medical and dental practices.1,2 Because it has no interaction with adrenergic receptors, it is suggested that FEL has fewer side effects than EPI.3 Hence, FEL causes fewer cardiovascular 4 and metabolic 5 side effects, and it has a higher median lethal dose (LD50) 6 than EPI. However, the mechanisms and the receptors used by FEL to induce cardiovascular effects are unknown, and very few studies have been conducted on its possible systemic effects.AVP, as opposed to FEL, has been widely studied. It acts on 2 subtypes of vasopressin receptors (V 1 and V 2 receptors). In physiological conditions, the vascular V 1 receptors promote vasoconstriction when linked to AVP. It has great importance because it helps control arterial pressure by enhancing it, mainly when a reduc- tion in blood volume occurs.3 Another physiological role for AVP occurs when it is associated with central V 1 receptors, inducing an increase in baroreflex gain (BG).7,8 BG may be defined as the degree of effectiveness to which the baroreflex maintains the arterial pressure at near-normal conditions, producing reflex bradycardia and vasodilation after a rapid arterial pressure elevation or permitting tachycardia and vasoconstriction after a decrease in arterial pressure.9 Injection of the V 1 receptor antagonist in the area postrema (AP) 10 or AP lesion 11 inhibits the ability of peripheral AVP to enhance BG. The V 2 receptors are present in the kidneys, and they promote water retention when they are linked to AVP. 3Because the FEL molecule is similar to the AVP molecule, it is possible that FEL activates cardiovascular mechanisms similar ...

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Central cardiovascular effects of AVP and ANP in normotensive and spontaneously hypertensive rats

Cited by 16 publications

References 39 publications

Vasopressin Acts in the Subfornical Organ to Decrease Blood Pressure

Vasopressin Acts in the Subfornical Organ to Decrease Blood Pressure

Atrial natriuretic peptide regulation of noradrenaline release in the anterior hypothalamic area of spontaneously hypertensive rats.

Cardiovascular Effects of Felypressin

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