Cardiac hypertrophy and brain natriuretic peptide in experimental hypertension

1994 ◽  
Vol 266 (2) ◽  
pp. R451-R457 ◽  
Author(s):  
M. Kohno ◽  
T. Fukui ◽  
T. Horio ◽  
K. Yokokawa ◽  
K. Yasunari ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Spontaneously Hypertensive Rats ◽  
Chronic Treatment ◽  
Experimental Hypertension ◽  
Acute Administration ◽  
Hypertensive Rats ◽  
Secretory Rate ◽  
Spontaneously Hypertensive

The blood pressure was decreased after chronic treatment with enalapril, MK-954, and hydralazine in deoxycorticosterone acetate (DOCA)-salt-induced malignant hypertension of spontaneously hypertensive rats (SHR); however, ventricular weight and plasma brain natriuretic peptide (BNP) concentration were decreased after enalapril and MK-954 but not after hydralazine. The BNP secretory rates from the ventricle in enalapril- and MK-954-treated DOCA-salt SHR were decreased to approximately 50% of those in untreated DOCA-salt SHR. The BNP secretory rate from the ventricle was positively correlated with ventricular weight in untreated and treated DOCA-salt SHR. In contrast, acute administration of captopril or MK-954 did not decrease the BNP secretory rate from the heart. Results suggest that the decrease in plasma BNP after enalapril and MK-954 is attributed to a decline in the secretion from the ventricle but not from the atrium. The reduction in ventricular mass appeared to be related to this decline.

Abstract 181: Overexpression of Arachidonic Acid Cytochrome P450 Expoxygenases Prevents the Development of High Blood Pressure via Enhancing Atrial Natriuretic Peptide in Spontaneously Hypertensive Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Dao Wen Wang ◽  
Bin Xiao ◽  
Yong Wang ◽  
Xiaojun Xiong ◽  
Darryl C Zeldin
Keyword(s):  
Blood Pressure ◽  
Cytochrome P450 ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Spontaneously Hypertensive Rats ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Atrial Natriuretic

Cytochrome P450 (CYP)-derived epoxyeicosatrienoic acids (EETs) have potent vasodilatory and diuretic feature, and therefore potentially hypotensive effect. No in vivo studies, however, were performed to support it. This study investigated the hypothesis via overexpressing CYP epoxygense genes in spontaneously hypertensive rats (SHR). Recombinant adeno-associated virus vector (rAAV) was utilized to mediate long-term transfection of CYP2J2 and CYP2C11 genes, respectively, in adult SHR, and animal systolic blood pressure (SBP) was monitored using arterial caudilis indirect manometric method. Results showed that at 2 months the urinary excretion of stable hydrolysis metabolic product of 14, 15-EE, 14–15-DHET increased by 11 and 8.7 folds in rAAV-2J2 and rAAV-2C11 groups, respectively, compared with AAV-GFP-treated rats. (2) SBP in 2J2- and 2C11-treated rats decreased from 175.0 ± 2.8mHg to 163.5 ± 5.8mmHg and 161.2 ± 6.1 mmHg, respectively, ( p <0.01) at month 2, and it is 165.0 ± 4.7 mmHg and 173.0 ± 12.8 mmHg at month 6 after gene injection (~30mmHg and ~23mmHg lowerer than that in control animals, respectively, p <0.001). (3) Before the rats were sacrificed, cardiac function tests with Pressure-Volume System showed that maximum intracardiac pressure was 202.1 ± 30.0 & 209.1 ± 17.1mmHg in two gene-treated rats, respectively, significantly lower than control (241.2 ± 18.2mmHg, p <0.01) and cardiac output in treatment rats were significantly higher than control (p<0.05). (4) Interestingly, atrial natriuretic peptide (ANP) mRNA were up-regulated 6–14 folds respectively in myocardium of 2J2 and 2C11 groups; furthermore, C-type receptor mRNA of ANP was increased in heart, lung, kidney and aorta. (5) in cultured atrial cells (HLB2G5), exogenous EETs stimulated ANP production. In conclusions, for first time our data indicates overexpression of CYP2J2 or CYP2C11 could prevent development of hypertension in SHR, improve cardiac functions, which may involve up-regulating ANP expression and its receptors in target tissues, which suppresses collagen deposition and cardiovascular remodeling.

scholarly journals Chronic treatment with tin normalizes blood pressure in spontaneously hypertensive rats.

Hypertension ◽  
1991 ◽  
Vol 17 (6_pt_1) ◽  
pp. 776-779 ◽  
Author(s):  
B Escalante ◽  
D Sacerdoti ◽  
M M Davidian ◽  
M Laniado-Schwartzman ◽  
J C McGiff
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Chronic Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Effect of Propranolol on Blood Pressure in Normal and Hypertensive Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 101s-103s
Author(s):  
J. Conway ◽  
K. Darwin ◽  
A. Hilditch ◽  
B. Loveday ◽  
M. Reeves
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Chronic Treatment ◽  
Spontaneous Hypertension ◽  
Beta Blockade ◽  
Experimental Hypertension ◽  
Hypertension Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Propranolol Treatment

1. Propranolol has been given orally in a dose sufficient to achieve beta-blockade throughout the day in normal rats, renal hypertensive animals with and without contralateral nephrectomy, spontaneously hypertensive and deoxycorticosterone (DOCA) hypertensive rats. The drug was given either after hypertension had become fully established or during the phase of rising blood pressure. 2. With this treatment, heart rate was reduced by approximately 100 beats/min in all experimental groups. 3. In established hypertension, treatment with propranolol for 7–9 days was ineffective in lowering blood pressure in any of the models of experimental hypertension. It also had no effect on blood pressure in normal animals. 4. Chronic treatment with propranolol during the phase of rising blood pressure had no effect in renal hypertensive animals. In spontaneous hypertension, the rise in blood pressure was limited to 28 mmHg with propranolol treatment as compared with 58 mmHg in control animals. Likewise, in DOCA hypertension, the rise in pressure was limited to 18 mmHg as compared with 46 mmHg in control animals.

scholarly journals Reconstitution of autophagy ameliorates vascular function and arterial stiffening in spontaneously hypertensive rats

2019 ◽  
Vol 317 (5) ◽  
pp. H1013-H1027 ◽  
Author(s):  
Cameron G. McCarthy ◽  
Camilla F. Wenceslau ◽  
Fabiano B. Calmasini ◽  
Nicole S. Klee ◽  
Michael W. Brands ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Function ◽  
Spontaneously Hypertensive Rats ◽  
Cellular Aging ◽  
Experimental Hypertension ◽  
Dependent Manner ◽  
Vascular Aging ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Autophagic Activity

Insufficient autophagy has been proposed as a mechanism of cellular aging, as this leads to the accumulation of dysfunctional macromolecules and organelles. Premature vascular aging occurs in hypertension. In fact, many factors that contribute to the deterioration of vascular function as we age are accelerated in clinical and experimental hypertension. Previously, we have reported decreased autophagy in arteries from spontaneously hypertensive rats (SHRs); however, the effects of restoring autophagic activity on blood pressure and vascular function are currently unknown. We hypothesized that reconstitution of arterial autophagy in SHRs would decrease blood pressure and improve endothelium-dependent relaxation. We treated 14- to 18-wk-old Wistar rats ( n = 7 vehicle and n = 8 trehalose) and SHRs ( n = 7/group) with autophagy activator trehalose (2% in drinking water) for 28 days. Blood pressure was measured by radiotelemetry, and vascular function and structure were measured in isolated mesenteric resistance arteries (MRAs) using wire and pressure myographs, respectively. Treatment with trehalose had no effect on blood pressure in SHRs; however, isolated MRAs presented enhanced relaxation to acetylcholine, in a cyclooxygenase- and reactive oxygen species-dependent manner. Similarly, trehalose treatment shifted the relaxation to the Rho kinase (ROCK) inhibitor Y-27632 to the right, indicating reduced ROCK activity. Finally, trehalose treatment decreased arterial stiffness as indicated by the slope of the stress-strain curve. Overall these data indicate that reconstitution of arterial autophagy in SHRs improves endothelial and vascular smooth muscle function, which could synergize to prevent stiffening. As a result, restoration of autophagic activity could be a novel therapeutic for premature vascular aging in hypertension. NEW & NOTEWORTHY This work supports the concept that diminished arterial autophagy contributes to premature vascular aging in hypertension and that therapeutic reconstitution of autophagic activity can ameliorate this phenotype. As vascular age is a new clinically used index for cardiovascular risk, understanding this mechanism may assist in the development of new drugs to prevent premature vascular aging in hypertension. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/behind-the-bench-episode-one-cam-squared/ .

Microvascular Effects of Echinodorus grandiflorus on Cardiovascular Disorders

Planta Medica ◽  
2020 ◽  
Vol 86 (06) ◽  
pp. 395-404 ◽  
Author(s):  
Fabiana Gomes ◽  
André M. Marques ◽  
Obadia Nathalie ◽  
Marcos Adriano Lessa ◽  
Eduardo Tibiriçá ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Chronic Treatment ◽  
Spontaneously Hypertensive Rat ◽  
Microvascular Blood Flow ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Anti Inflammatory ◽  
The Brain

Abstract Echinodorus grandiflorus is a semiaquatic plant native to Brazil and belongs to the Alismataceae family. Infusion preparations of the leaves of this plant are often used due to its diuretic, blood pressure lowering, and anti-inflammatory properties. Our aim was to investigate the effects of chronic treatment with the crude hydroalcoholic extract of E. grandiflorus on central and peripheral microvascular changes induced in a model of hypertension and diabetes. The hemodynamic and microvascular effects of E. grandiflorus extract (50, 100, or 200 mg/kg/day for 28 days) or the isolated major diterpene from E. grandiflorus (3 to 10 mg/kg i. v.) were evaluated in spontaneously hypertensive rats using tail plethysmography and intravital fluorescence videomicroscopy, respectively, and were compared to vehicle-treated normotensive Wistar-Kyoto rats. We also investigated the protective effects of chronic treatment with E. grandiflorus (100 mg/kg/day) in brain capillary density and leukocyte-endothelium interactions on the brain vessels of DM-spontaneously (DM: diabetes mellitus) hypertensive rats. Chronically treating spontaneously hypertensive rats with increasing doses of crude hydroalcoholic E. grandiflorus extract resulted in significant dose-dependent reductions in systolic blood pressure and an anti-inflammatory effect on the brain microcirculation of DM-spontaneously hypertensive rat animals. Using laser speckle contrast imaging, we observed that intravenous administration of the major isolated clerodane diterpene metabolite (1 – 10 mg/kg) increased microvascular blood flow by 25% in spontaneously hypertensive rat skeletal muscle. The results of this study show that E. grandiflorus extracts can be useful in the prevention and reduction of microcirculatory damage in arterial hypertension and other diseases that involve microvascular dysfunction.

scholarly journals Acute Blood Pressure, Renal and cGMP Responses to the Novel Designer Natriuretic Peptide ZD100 in Spontaneously Hypertensive Rats

2015 ◽  
Vol 21 (8) ◽  
pp. S1
Author(s):  
Alessia Buglioni ◽  
Jeson S. Sangaralingham ◽  
Gerald E. Harders ◽  
Brenda K. Huntley ◽  
Horng H. Chen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Natriuretic Peptide ◽  
Spontaneously Hypertensive Rats ◽  
The Novel ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Renal actions of atrial natriuretic peptide in spontaneously hypertensive rats: the role of nitric oxide as a key mediator

2012 ◽  
Vol 302 (11) ◽  
pp. F1385-F1394 ◽  
Author(s):  
Rosana Elesgaray ◽  
Carolina Caniffi ◽  
Lucía Savignano ◽  
Mariana Romero ◽  
Myriam Mac Laughlin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Calmodulin Inhibitors ◽  
Nos Isoforms ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) is an important regulator of blood pressure (BP). One of the mechanisms whereby ANP impacts BP is by stimulation of nitric oxide (NO) production in different tissues involved in BP control. We hypothesized that ANP-stimulated NO is impaired in the kidneys of spontaneously hypertensive rats (SHR) and this contributes to the development and/or maintenance of high levels of BP. We investigated the effects of ANP on the NO system in SHR, studying the changes in renal nitric oxide synthase (NOS) activity and expression in response to peptide infusion, the signaling pathways implicated in the signaling cascade that activates NOS, and identifying the natriuretic peptide receptors (NPR), guanylyl cyclase receptors (NPR-A and NPR-B) and/or NPR-C, and NOS isoforms involved. In vivo, SHR and Wistar-Kyoto rats (WKY) were infused with saline (0.05 ml/min) or ANP (0.2 μg·kg−1·min−1). NOS activity and endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) NOS expression were measured in the renal cortex and medulla. In vitro, ANP-induced renal NOS activity was determined in the presence of iNOS and nNOS inhibitors, NPR-A/B blockers, guanine nucleotide-regulatory (Gi) protein, and calmodulin inhibitors. Renal NOS activity was higher in SHR than in WKY. ANP increased NOS activity, but activation was lower in SHR than in WKY. ANP had no effect on expression of NOS isoforms. ANP-induced NOS activity was not modified by iNOS and nNOS inhibitors. NPR-A/B blockade blunted NOS stimulation via ANP in kidney. The renal NOS response to ANP was reduced by Gi protein and calmodulin inhibitors. We conclude that ANP interacts with NPR-C, activating Ca-calmodulin eNOS through Gi protein. NOS activation also involves NPR-A/B. The NOS response to ANP was diminished in kidneys of SHR. The impaired NO system response to ANP in SHR participates in the maintenance of high blood pressure.

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