Influence of Arginine Vasopressin Receptor and Nitric Oxide on the Water, Sodium Intake and Arterial Blood Pressure Induce by Angiotensin Injected into Third Ventricle of the Brain

Sodium supplementation given for 1 wk to nonpregnant rats induces changes that are adequate to maintain renal and circulatory homeostasis as well as arterial blood pressure. However, in pregnant rats, proteinuria, fetal growth restriction, and placental oxidative stress are observed. Moreover, the decrease in blood pressure and expansion of circulatory volume, normally associated with pregnancy, are prevented by high-sodium intake. We hypothesized that, in these pregnant rats, a loss of the balance between prooxidation and antioxidation, particularly in kidneys and heart, disturbs the normal course of pregnancy and leads to manifestations such as gestational hypertension. We thus investigated the presence of oxidative/nitrosative stress in heart and kidneys following high-sodium intake in pregnant rats. Markers of this stress [8-isoprostaglandin F2α (8-iso-PGF2α) and nitrotyrosine], producer of nitric oxide [nitric oxide synthases (NOSs)], and antioxidants [superoxide dismutase (SOD) and catalase] were measured. Then, molecules (Na+-K+-ATPase and aconitase) or process [apoptosis (Bax and Bcl-2), inflammation (monocyte chemoattractant protein-1, connective tissue growth factor, and TNF-α)] susceptible to free radicals was determined. In kidneys from pregnant rats on 1.8% NaCl-water, NOSs, apoptotic index, and nitrotyrosine expression were increased, whereas Na+-K+-ATPase mRNA and activity were decreased. In the left cardiac ventricle of these rats, heightened nitrotyrosine, 8-iso-PGF2α, and catalase activity together with reduced endothelial NOS protein expression and SOD and aconitase activities were observed. These findings suggest that oxidative/nitrosative stress in kidney and left cardiac ventricle destabilizes the normal course of pregnancy and could lead to gestational hypertension.

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Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1979.237.3.h381 ◽

1979 ◽

Vol 237 (3) ◽

pp. H381-H385 ◽

Cited By ~ 4

Author(s):

E. F. Ellis ◽

E. P. Wei ◽

H. A. Kontos

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Arterial Blood Pressure ◽

Standard Error ◽

Arterial Blood ◽

Cerebral Arterioles ◽

The Mean ◽

Dose Dependent ◽

The Brain

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

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Chronic Endothelium-Dependent Regulation of Arterial Blood Pressure by Atrial Natriuretic Peptide: Role of Nitric Oxide and Endothelin-1

Endocrinology ◽

10.1210/en.2008-1360 ◽

2009 ◽

Vol 150 (5) ◽

pp. 2382-2387 ◽

Cited By ~ 11

Author(s):

Karim Sabrane ◽

Markus-N. Kruse ◽

Alexandra Gazinski ◽

Michaela Kuhn

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Methyl Ester ◽

Atrial Natriuretic Peptide ◽

Arterial Blood Pressure ◽

Natriuretic Peptide ◽

Endothelin 1 ◽

Arterial Blood ◽

Atrial Natriuretic

Atrial natriuretic peptide (ANP), via its guanylyl cyclase (GC)-A receptor, plays a key role in the regulation of arterial blood pressure (ABP) and volume. Endothelial-restricted deletion of GC-A in mice [endothelial cell (EC) GC-A knockout (KO)] resulted in hypervolemic hypertension, demonstrating that the endothelium participates in the hypotensive and hypovolemic actions of ANP. Published studies showed that ANP modulates the release of the vasoactive factors nitric oxide (NO) and endothelin-1 (ET-1) from cultured endothelia. Based on these observations, we examined the role of these endothelial factors in ANP-dependent vasodilatation (studied in isolated arteries) and chronic regulation of ABP (measured in awake mice by tail-cuff plethysmography). ANP induced concentration-dependent vasorelaxations of aortic, carotid, and pulmonary arteries. These responses were not different between control and EC GC-A KO mice, and were significantly enhanced after inhibition of NO synthase [by N(G)-nitro-l-arginine-methyl ester]. Intravenous administration of N(G)-nitro-l-arginine-methyl ester to conscious mice significantly increased ABP. The extent of these hypertensive reactions was similar in EC GC-A KO mice and control littermates (increases in systolic blood pressure by ∼25 mm Hg). Conversely, antagonism of ET-1/endothelin-A receptors with BQ-123 reduced ABP significantly and comparably in both genotypes (by ∼11 mm Hg). Finally, the vascular and tissue expression levels of components of the NO system and of immunoreactive ET-1 were not different in control and EC GC-A KO mice. We conclude that the endothelium, but not modulation of endothelial NO or ET-1, participates in the chronic regulation of ABP by ANP.

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Cerebral Blood Flow Changes during Cortical Spreading Depression are Not Altered by Inhibition of Nitric Oxide Synthesis

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1994.125 ◽

1994 ◽

Vol 14 (6) ◽

pp. 939-943 ◽

Cited By ~ 31

Author(s):

Zheng Gang Zhang ◽

Michael Chopp ◽

Kenneth I. Maynard ◽

Michael A. Moskowitz

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Arterial Blood Pressure ◽

Cortical Spreading Depression ◽

Spreading Depression ◽

Arterial Blood ◽

Nos Inhibitors ◽

Before And After ◽

Male Wistar Rats

CBF increases concomitantly with cortical spreading depression (CSD). We tested the hypothesis that CBF changes during CSD are mediated by nitric oxide (NO). Male Wistar rats (n = 23) were subjected to KCl-induced CSD before and after administration of nitric oxide synthase (NOS) inhibitors N-nitro-l-arginine (L-NNA) or N-nitro-l-arginine methyl ester (L-NAME) and in nontreated animals. CBF, CSD, and mean arterial blood pressure were recorded. Brain NOS activity was measured in vitro in control, L-NNA, and L-NAME-treated rats by the conversion of [3H]arginine to [3H]citrulline. Our data show that the NOS inhibitors did not significantly change regional CBF (rCBF) during CSD, even though cortical NOS activity was profoundly depressed and systemic arterial blood pressure was significantly increased. Our data suggest that rCBF during CSD in rats is not regulated by NO.

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Relationship between Arterial Blood Pressure and Dietary Sodium Intake in Subjects with and without a Familial Predisposition to Hypertension

Clinical Science ◽

10.1042/cs061030p ◽

1981 ◽

Vol 61 (3) ◽

pp. 30P-30P

Author(s):

P.S. Parfrey ◽

C.R. Lee ◽

N.D. Markandu ◽

J.E. Roulston ◽

M. Squires ◽

...

Keyword(s):

Blood Pressure ◽

Arterial Blood Pressure ◽

Sodium Intake ◽

Dietary Sodium ◽

Familial Predisposition ◽

Arterial Blood

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Dietary Sodium Intake and Arterial Blood Pressure

Journal of Renal Nutrition ◽

10.1053/j.jrn.2008.10.006 ◽

2009 ◽

Vol 19 (1) ◽

pp. 57-60 ◽

Cited By ~ 26

Author(s):

Francis Dumler

Keyword(s):

Blood Pressure ◽

Arterial Blood Pressure ◽

Sodium Intake ◽

Dietary Sodium ◽

Arterial Blood

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Arterial Blood Pressure Responses to Cell-free Hemoglobin Solutions and the Reaction with Nitric Oxide

Journal of Biological Chemistry ◽

10.1074/jbc.273.20.12128 ◽

1998 ◽

Vol 273 (20) ◽

pp. 12128-12134 ◽

Cited By ~ 231

Author(s):

Ronald J. Rohlfs ◽

Eric Bruner ◽

Albert Chiu ◽

Armando Gonzales ◽

Maria L. Gonzales ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Arterial Blood Pressure ◽

Free Hemoglobin ◽

Arterial Blood ◽

Blood Pressure Responses

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Pituitary-Adrenocortical Function and Experimental Inherited Hypertension: Perspectives of Permanent Correction

Physiology ◽

10.1152/physiologyonline.1994.9.1.7 ◽

1994 ◽

Vol 9 (1) ◽

pp. 7-11

Author(s):

EV Naumenko

Keyword(s):

Blood Pressure ◽

Arterial Blood Pressure ◽

Early Ontogenesis ◽

Adrenocortical Function ◽

System A ◽

Arterial Blood ◽

Norepinephrine Metabolism ◽

The Brain ◽

Adrenocortical System ◽

Noradrenergic Mechanism

Changes of pituitary-adrenocortical function in rats with inherited hypertension are associated with alteration of the brain noradrenergic mechanism regulating both arterial blood pressure and the adrenocortical system. A way of permanent restoration of blood pressure and adrenocortical function by interference into norepinephrine metabolism in early ontogenesis is discovered.

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