[PP.06.12] B-TYPE NATRIURETIC PEPTIDE IS A DETERMINANT OF THE NOCTURNAL INCREASE IN BLOOD PRESSURE INDEPENDENTLY OF ARTERIAL HYPERTROPHY AND HYPOXIA

We investigated whether the effect of long-term intermittent hypoxia (LTIH) on cardiovascular function may be modified by preexisting genetic traits. To induce LTIH experimentally, cycles of 90-s hypoxia (nadir 6%) followed by 90-s normoxia were applied to six Wistar-Kyoto and six spontaneously hypertensive rats during 8 h daily. Comparison with the same number of control animals after 70 days revealed no alteration of intra-arterial blood pressure or heart rate. Blood pressure responsiveness to a brief hypoxic stimulus was enhanced in the LTIH animals, regardless of strain, whereas the hypoxia-induced increase in heart rate was abolished. In the spontaneously hypertensive but not the Wistar-Kyoto rats, LTIH increased left ventricular weight-to-body weight ratio and content of atrial natriuretic peptide mRNA. Expression of B-type natriuretic peptide was unchanged (Northern blot). Slightly increased right ventricular weight-to-body weight ratios in the LTIH animals were associated with higher right ventricular atrial natriuretic peptide and B-type natriuretic peptide mRNA amounts. Consequently, the effects of LTIH on different components of cardiovascular function appear incompletely related to each other and differentially influenced by constitutional traits.

Download Full-text

Renin and atrial natriuretic peptide restriction fragment length polymorphisms: association with ethnicity and blood pressure

Journal of Hypertension ◽

10.1097/00004872-199111000-00003 ◽

1991 ◽

Vol 9 (11) ◽

pp. 993-996 ◽

Cited By ~ 59

Author(s):

Jacqueline Barley ◽

Nicholas D. Carter ◽

J Kennedy Cruickshank ◽

Stephen Jeffery ◽

Alberto Smith ◽

...

Keyword(s):

Blood Pressure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Restriction Fragment ◽

Fragment Length ◽

Restriction Fragment Length Polymorphisms ◽

Length Polymorphisms ◽

Restriction Fragment Length ◽

Atrial Natriuretic

Download Full-text

Atrial natriuretic peptide and adaptation of sodium urinary excretion in patients with chronic renal failure

Clinical Science ◽

10.1042/cs0750243 ◽

1988 ◽

Vol 75 (3) ◽

pp. 243-249 ◽

Cited By ~ 10

Author(s):

Stanislas Czekalski ◽

Catherine Michel ◽

Jean-Claude Dussaule ◽

Philippe Touraine ◽

Francoise Mignon ◽

...

Keyword(s):

Blood Pressure ◽

Renal Failure ◽

Chronic Renal Failure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Sodium Excretion ◽

Mean Blood Pressure ◽

Group Iii ◽

Sodium Load ◽

Atrial Natriuretic

1. In order to examine the potential role of endogenous atrial natriuretic peptide (ANP) in modulating the increased sodium excretion per nephron in chronic renal failure, we studied healthy subjects with normal renal function (group I) and patients with moderate (group II) or severe chronic renal failure (group III) before, during and after administration of an intravenous sodium load. All subjects had been on a controlled diet containing 120 mmol of sodium per day for 5 days before the study. 2. Under basal conditions, plasma ANP and fractional excretion of sodium (FENa) were highest in group III. Both parameters increased in response to the sodium load in the three groups studied (P < 0.001). Changes with time differed from group to group (P < 0.05), the more marked response for both parameters being observed in group III. After adjustment with respect to plasma ANP (analysis of covariance), FENa was no longer modified in response to the sodium load, whereas adjustment of FENa with respect to mean blood pressure was without consequence on the significance of its change with time. This demonstrates that plasma ANP, but not mean blood pressure, represents the main factor producing variation in FENa during and after the sodium load. 3. These results suggest an important role for plasma ANP in promoting adaptation of short-term sodium excretion in response to an acute sodium load in patients with chronic renal failure who ingest a normal sodium intake.

Download Full-text

Centella asiatica (L.) Urb. Prevents Hypertension and Protects the Heart in Chronic Nitric Oxide Deficiency Rat Model

Frontiers in Pharmacology ◽

10.3389/fphar.2021.742562 ◽

2021 ◽

Vol 12 ◽

Author(s):

Mohd Khairulanwar Bunaim ◽

Yusof Kamisah ◽

Mohd Noor Mohd Mustazil ◽

Japar Sidik Fadhlullah Zuhair ◽

Abdul Hamid Juliana ◽

...

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Brain Natriuretic Peptide ◽

Natriuretic Peptide ◽

Rat Model ◽

Antioxidant Properties ◽

Centella Asiatica ◽

Sprague Dawley ◽

Cardiac Damage ◽

Ace Activity

Background: Hypertension is a major risk factor for cardiovascular disease (CVD), which is the number one cause of global mortality. The potential use of natural products to alleviate high blood pressure has been demonstrated to exert a cardioprotective effect. Centella asiatica (L.) Urb. belongs to the plant family Apiaceae (Umbelliferae). It contains a high amount of triterpenoid and flavonoid that have antioxidant properties and are involved in the renin-angiotensin-aldosterone system which is an important hormonal system for blood pressure regulation.Objective: This study aimed to investigate the effects of C. asiatica ethanolic extract on blood pressure and heart in a hypertensive rat model, which was induced using oral N(G)-nitro-l-arginine methyl ester (l-NAME).Methods: Male Sprague-Dawley rats were divided into five groups and were given different treatments for 8 weeks. Group 1 only received deionized water. Groups 2, 4, and 5 were given l-NAME (40 mg/kg, orally). Groups 4 and 5 concurrently received C. asiatica extract (500 mg/kg, orally) and captopril (5 mg/kg, orally), respectively. Group 3 only received C. asiatica extract (500 mg/kg body weight, orally). Systolic blood pressure (SBP) was measured at weeks 0, 4, and 8, while serum nitric oxide (NO) was measured at weeks 0 and 8. At necropsy, cardiac and aortic malondialdehyde (MDA) contents, cardiac angiotensin-converting enzyme (ACE) activity, and serum level of brain natriuretic peptide (BNP) were measured.Results: After 8 weeks, the administrations of C. asiatica extract and captopril showed significant (p < 0.05) effects on preventing the elevation of SBP, reducing the serum nitric oxide level, as well as increasing the cardiac and aortic MDA content, cardiac ACE activity, and serum brain natriuretic peptide level.Conclusion:C. asiatica extract can prevent the development of hypertension and cardiac damage induced by l-NAME, and these effects were comparable to captopril.

Download Full-text

Molecular and genetic aspects of guanylyl cyclase natriuretic peptide receptor-A in regulation of blood pressure and renal function

Physiological Genomics ◽

10.1152/physiolgenomics.00083.2018 ◽

2018 ◽

Vol 50 (11) ◽

pp. 913-928 ◽

Cited By ~ 10

Author(s):

Kailash N. Pandey

Keyword(s):

Blood Pressure ◽

Natriuretic Peptide ◽

Guanylyl Cyclase ◽

Natriuretic Peptides ◽

Molecular Mechanisms ◽

Phenotypic Characterization ◽

Natriuretic Peptide Receptor ◽

Peptide Receptor ◽

Natriuretic Peptide Receptor A ◽

Regulation Of Blood Pressure

Natriuretic peptides (NPs) exert diverse effects on several biological and physiological systems, such as kidney function, neural and endocrine signaling, energy metabolism, and cardiovascular function, playing pivotal roles in the regulation of blood pressure (BP) and cardiac and vascular homeostasis. NPs are collectively known as anti-hypertensive hormones and their main functions are directed toward eliciting natriuretic/diuretic, vasorelaxant, anti-proliferative, anti-inflammatory, and anti-hypertrophic effects, thereby, regulating the fluid volume, BP, and renal and cardiovascular conditions. Interactions of NPs with their cognate receptors display a central role in all aspects of cellular, biochemical, and molecular mechanisms that govern physiology and pathophysiology of BP and cardiovascular events. Among the NPs atrial and brain natriuretic peptides (ANP and BNP) activate guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA) and initiate intracellular signaling. The genetic disruption of Npr1 (encoding GC-A/NPRA) in mice exhibits high BP and hypertensive heart disease that is seen in untreated hypertensive subjects, including high BP and heart failure. There has been a surge of interest in the NPs and their receptors and a wealth of information have emerged in the last four decades, including molecular structure, signaling mechanisms, altered phenotypic characterization of transgenic and gene-targeted animal models, and genetic analyses in humans. The major goal of the present review is to emphasize and summarize the critical findings and recent discoveries regarding the molecular and genetic regulation of NPs, physiological metabolic functions, and the signaling of receptor GC-A/NPRA with emphasis on the BP regulation and renal and cardiovascular disorders.

Download Full-text