Relationship between thirst and diazoxide-induced hypotension in rats

1990 ◽  
Vol 259 (2) ◽  
pp. R362-R370 ◽  
Author(s):  
M. D. Evered
Keyword(s):  
Angiotensin Ii ◽  
Venous Pressure ◽  
Plasma Osmolality ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Induced Hypotension ◽  
Potent Vasodilator ◽  
K Concentration ◽  
The Relationship ◽  
Dose Dependent

Diazoxide, a potent vasodilator and antidiuretic, was used to examine the relationship between hypotension and thirst in conscious rats with indwelling arterial and venous catheters. Bolus iv. injections (5-50 mg/kg) caused prompt, long-lasting, and dose-dependent reductions in mean arterial pressure (MAP) and stimulated drinking. Water intake and degree of hypotension were closely correlated when MAP was 10-65 mmHg below normal. At the time of drinking there were no significant changes in central venous pressure, plasma osmolality, or Na+ or K+ concentration. Plasma glucose increased approximately 35%, and blood volume increased approximately 10% (based on hematocrit changes and dilution of Evans blue). Captopril (100 mg/kg sc to block the renin-angiotensin system) enhanced the depressor response to diazoxide but abolished the dipsogenic response over the same range of arterial pressures tested in controls. Angiotensin II iv infusion restored drinking in captopril-treated animals. The combination of captopril and diazoxide did not block drinking to iv infusions of hypertonic saline or water deprivation. These results confirm that hypotension potently stimulates thirst and support the hypothesis that angiotensin II mediates the dipsogenic response in rats.

Centrally induced cardiovascular and sympathetic responses to hydrocortisone in rats

1983 ◽  
Vol 245 (6) ◽  
pp. H1013-H1018 ◽  
Author(s):  
H. Takahashi ◽  
K. Takeda ◽  
H. Ashizawa ◽  
A. Inoue ◽  
S. Yoneda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Angiotensin Ii Antagonist ◽  
Dose Dependent

Central effects of hydrocortisone were investigated by injecting it intracerebroventricularly (icv) while recording blood pressure and heart rate in awake rats. Dose-dependent increases in both blood pressure and heart rate occurred following injections of hydrocortisone. Pretreatment by icv injections of the angiotensin II antagonist, [Sar1-Ile8]angiotensin II, completely abolished vasopressor responses to subsequent injections of hydrocortisone. When rats were later anesthetized with urethan to allow recording of abdominal sympathetic nerve activity, hydrocortisone produced vasopressor responses accompanied by corresponding increases in sympathetic nerve firing, which were also abolished by central pretreatment with either [Sar1-Ile8]angiotensin II or angiotensin I converting-enzyme inhibitor, captopril. These results indicate that centrally administered hydrocortisone stimulates the brain renin-angiotensin system to produce vasopressor responses by increasing sympathetic nerve firing.

scholarly journals High intraluminal pressure via H2O2 upregulates arteriolar constrictions to angiotensin II by increasing the functional availability of AT1 receptors

2008 ◽  
Vol 295 (2) ◽  
pp. H835-H841 ◽  
Author(s):  
Zsolt Bagi ◽  
Nora Erdei ◽  
Akos Koller
Keyword(s):  
High Pressure ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Intraluminal Pressure ◽  
Ang Ii ◽  
At1 Receptors ◽  
Angiotensin System ◽  
Dose Dependent

Previously, we found that high intraluminal pressure leads to production of reactive oxygen species (ROS) and also upregulates several components of the renin-angiotensin system in the wall of small arteries. We hypothesized that acute exposure of arterioles to high intraluminal pressure in vitro via increasing ROS production enhances the functional availability of type 1 angiotensin II (Ang II) receptors (AT1 receptors), resulting in sustained constrictions. In arterioles (∼180 μm) isolated from rat skeletal muscle, Ang II elicited dose-dependent constrictions, which decreased significantly by the second application [maximum (max.): from 59% ± 4% to 26% ± 5% at 10−8 M; P < 0.05] in the presence of 80 mmHg of intraluminal pressure. In contrast, if the arterioles were exposed to high intraluminal pressure (160 mmHg for 30 min), Ang II-induced constrictions remained substantial on the second application (max.: 51% ± 3% at 10−8 M). In the presence of Tiron and polyethylene glycol (PEG)-catalase, known to reduce the level of superoxide anion and hydrogen peroxide (H2O2), second applications of Ang II evoked similarly reduced constrictions, even after high-pressure exposure (29% ± 4% at 10−8 M). Furthermore, when arterioles were exposed to H2O2 (for 30 min, 10−7 M, at normal 80 mmHg pressure), Ang II-induced constrictions remained substantial on second applications (59% ± 5% at 10−8 M). These findings suggest that high pressure, likely via inducing H2O2 production, increases the functional availability of AT1 receptors and thus enhances Ang II-induced arteriolar constrictions. We propose that in hypertension–regardless of etiology–high intraluminal pressure, via oxidative stress, enhances the functional availability of AT1 receptors augmenting Ang II-induced constrictions.

scholarly journals Obesity, essential hypertension and renin–angiotensin system

2007 ◽  
Vol 10 (10A) ◽  
pp. 1151-1155 ◽  
Author(s):  
Julian Segura ◽  
Luis M Ruilope
Keyword(s):  
Essential Hypertension ◽  
Insulin Sensitivity ◽  
Angiotensin Ii ◽  
Antihypertensive Drugs ◽  
Renin Angiotensin System ◽  
Overweight And Obesity ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Relationship

AbstractAbdominal obesity is a risk factor for cardiovascular disease worldwide, and it is becoming a dramatic issue for national health systems. Overweight and obesity are highly associated with multiple comorbidities, elevated blood pressure values, dyslipidaemia, reduced insulin sensitivity and alterations of large and minor vessels.Activation of the renin–angiotensin system (RAS) in adipose tissue may represent an important link between obesity and hypertension. Angiotensin II has been shown to play a role in adipocyte growth and differentiation. Adipocytes also secrete adiponectin, enhancing insulin sensitivity and preventing atherosclerosis. Blockade of the RAS with either an angiotensin-converting enzyme inhibitor or an angiotensin II receptor blocker results in a substantial increase in adiponectin levels and improved insulin sensitivity. Obesity-related hypertension needs a comprehensive approach to treatment including both weight loss and pharmacological therapies. Antihypertensive drugs prescription should be based on guidelines recommendations for management of hypertension, taking into account the growing evidences about the relationship between some antihypertensive drugs and the development of new-onset diabetes.This review discusses the role of RAS in the relationship between obesity, essential hypertension and insulin resistance.

scholarly journals Minireview: Overview of the Renin-Angiotensin System—An Endocrine and Paracrine System

Endocrinology ◽  
2003 ◽  
Vol 144 (6) ◽  
pp. 2179-2183 ◽  
Author(s):  
Julie L. Lavoie ◽  
Curt D. Sigmund
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Active Component ◽  
Renin Angiotensin System ◽  
Transgenic Animals ◽  
Causative Factor ◽  
Transgenic Models ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Relationship

Abstract Since the discovery of renin as a pressor substance in 1898, the renin-angiotensin (RAS) system has been extensively studied because it remains a prime candidate as a causative factor in the development and maintenance of hypertension. Indeed, some of the properties of the physiologically active component of the RAS, angiotensin II, include vasoconstriction, regulation of renal sodium and water absorption, and increasing thirst. Initially, its affect on blood pressure was thought to be mediated primarily through the classical endocrine pathway; that is, the generation of blood-borne angiotensin with actions in target tissues. More recently, however, it has become appreciated that a local autocrine or paracrine RAS may exist in a number of tissues, and that these may also play a significant role in regulating blood pressure. Some of the difficulties in studying tissue RAS stem from the limitations of pharmacology in not differentiating between RAS products made systemically from those synthesized locally. However, the development of transgenic animals with highly specific promoters to target the RAS to specific tissues provided important tools to dissect these systems. Thus, this minireview will discuss recent advances in understanding the relationship between endocrine and paracrine (tissue) RAS using transgenic models.

A Review of Angiotensin Receptor Blocker-based Therapies at all Levels of Cardiovascular Risk

2011 ◽  
Vol 7 (4) ◽  
pp. 254 ◽  
Author(s):  
Giuliano Tocci ◽  
Lorenzo Castello ◽  
Massimo Volpe ◽  
◽  
◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Ventricular Hypertrophy ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Clinical Settings ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Receptor Blockers ◽  
Artery Disease

The renin–angiotensin system (RAS) has a key role in the maintenance of cardiovascular homeostasis, and water and electrolyte metabolism in healthy subjects, as well as in several diseases including hypertension, left ventricular hypertrophy and dysfunction, coronary artery disease, renal disease and congestive heart failure. These conditions are all characterised by abnormal production and activity of angiotensin II, which represents the final effector of the RAS. Over the last few decades, accumulating evidence has demonstrated that antihypertensive therapy based on angiotensin II receptor blockers (ARBs) has a major role in the selective antagonism of the main pathological activities of angiotensin II. Significant efforts have been made to demonstrate that blocking the angiotensin II receptor type 1 (AT1) subtype receptors through ARB-based therapy results in proven benefits in different clinical settings. In this review, we discuss the main benefits of antihypertensive strategies based on ARBs in terms of their efficacy, safety and tolerability.

scholarly journals Pathological Role of Angiotensin II in Severe COVID-19

TH Open ◽  
2020 ◽  
Vol 04 (02) ◽  
pp. e138-e144 ◽  
Author(s):  
Wolfgang Miesbach
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Treatment Options ◽  
Renin Angiotensin System ◽  
Target Cells ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Novel Coronavirus

AbstractThe activated renin–angiotensin system induces a prothrombotic state resulting from the imbalance between coagulation and fibrinolysis. Angiotensin II is the central effector molecule of the activated renin–angiotensin system and is degraded by the angiotensin-converting enzyme 2 to angiotensin (1–7). The novel coronavirus infection (classified as COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as acute respiratory distress syndrome, sepsis, and death in a proportion of patients, mostly elderly patients with preexisting comorbidities. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to enter the target cells, resulting in activation of the renin–angiotensin system. After downregulating the angiotensin-converting enzyme 2, the vasoconstrictor angiotensin II is increasingly produced and its counterregulating molecules angiotensin (1–7) reduced. Angiotensin II increases thrombin formation and impairs fibrinolysis. Elevated levels were strongly associated with viral load and lung injury in patients with severe COVID-19. Therefore, the complex clinical picture of patients with severe complications of COVID-19 is triggered by the various effects of highly expressed angiotensin II on vasculopathy, coagulopathy, and inflammation. Future treatment options should focus on blocking the thrombogenic and inflammatory properties of angiotensin II in COVID-19 patients.

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