Nebivolol Increases Atrial Natriuretic Peptide/Systolic Blood Pressure Ratio in Hypertensive Patients

2008 ◽  
Vol 6 (1) ◽  
pp. 31-35
Author(s):  
P.C. Papadopoulos ◽  
B. Kokkas ◽  
P. Kotridis ◽  
G. Aidonidis ◽  
V. Koutsimanis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Systolic Blood Pressure ◽  
Natriuretic Peptide ◽  
Pressure Ratio ◽  
Hypertensive Patients ◽  
Atrial Natriuretic

Effects of Moxibustion on Blood Pressure and Renal Function in Spontaneously Hypertensive Rats

1997 ◽  
Vol 25 (01) ◽  
pp. 21-26 ◽  
Author(s):  
Ho Sub Lee ◽  
Yun Cho Yu ◽  
Seong Tae Kim ◽  
Kyung Sik Kim
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Atrial Natriuretic Peptide ◽  
Systolic Blood Pressure ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Atrial Natriuretic

The aim of this study was to investigate the effects of moxibustion at the meridian points BL-15 (Xin-shu) and BL-27 (Xiao-chang-shu) on renal function, systolic blood pressure, plasma levels of renin activity, aldosterone and atrial natriuretic peptide in spontaneously hypertensive rats. The results showed that urine volume increased significantly after moxibustion at the meridian points BL-15, but decreased at BL-27. Urinary excretion of Na + decreased after moxibustion at the meridian points BL-15 and BL-27. Systolic blood pressure decreased after moxibustion at the meridian point BL-15. No effect was observed at BL-27. Plasma levels of aldosterone and renin activity increased significantly, but the levels of atrial natriuretic peptide decreased significantly after moxibustion at BL-15. Plasma levels of aldosterone and atrial natriuretic peptide increased significantly after moxibustion at the meridian points BL-27. These results suggest that the meridian points BL-15 and BL-27 are related to the regulation of renal function and the secretion of hormone with body fluid metabolism.

Passive heat exposure leads to delayed increase in plasma levels of atrial natriuretic peptide in humans

1991 ◽  
Vol 71 (2) ◽  
pp. 716-720 ◽  
Author(s):  
J. Leppaluoto ◽  
O. Arjamaa ◽  
O. Vuolteenaho ◽  
H. Ruskoaho
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Atrial Natriuretic Peptide ◽  
Systolic Blood Pressure ◽  
Natriuretic Peptide ◽  
Heat Exposure ◽  
Plasma Renin ◽  
Evaporative Water ◽  
Plasma Arginine ◽  
Atrial Natriuretic

The effects of passive heat exposure on atrial natriuretic peptide (ANP) were studied in six healthy men staying in a Finnish sauna at +92 degrees C for 20 min. Their rectal temperature increased by 0.4 degrees C, and evaporative water loss was 0.92 +/- 0.14 (SD) kg. Heart rate and systolic blood pressure increased significantly during the 20-min exposure. Serum osmolality and plasma arginine vasopressin levels increased during the exposure, then declined, and increased significantly again at 90–120 min. Plasma renin activity and aldosterone increased by two- to fourfold in 20 min. Plasma ANP levels rose from 13 +/- 7 to 39 +/- 15 ng/l at 60 min and to 41 +/- 13 ng/l at 120 min (P less than 0.01 for both). We conclude that transient increases in heart rate and systolic blood pressure or changes in blood volume as inferred from the weight loss do not contribute to the increased plasma ANP levels observed after the heat exposure. Instead, increased secretions of pressor hormones could explain the elevated plasma ANP levels observed after the thermal stress.

Fluid, Ionic and Hormonal Changes Induced by High Salt Intake in Salt-Sensitive and Salt-Resistant Hypertensive Patients

1996 ◽  
Vol 91 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Alejandro De La Sierra ◽  
María Del Mar Lluch ◽  
Antonio Coca ◽  
María Teresa Aguilera ◽  
Vicente Giner ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Salt Intake ◽  
Plasma Aldosterone ◽  
High Salt ◽  
Plasma Noradrenaline ◽  
Hypertensive Patients ◽  
High Salt Intake ◽  
Atrial Natriuretic

1. The aim of the study was to detect differences between salt-sensitive and salt-resistant hypertensive patients in the response of the renin—aldosterone axis, plasma noradrenaline and atrial natriuretic peptide to high salt intake. 2. Fifty essential hypertensive patients followed 2 weeks of a standard diet with 20 mmol of NaCl daily, supplemented by placebo tablets for the first 7 days and by NaCl tablets for the last 7 days, in a single-blind fashion. Salt sensitivity was defined as a significant rise (P < 0.05) in 24 h mean blood pressure obtained by ambulatory blood pressure monitoring from the low- to the high-salt period. Biochemical and hormonal measurements were performed on the last day of both periods. 3. Twenty-two (44%) patients fulfilled criteria of salt-sensitive hypertension, whereas the remaining 28 (56%) were considered salt-resistant. High salt intake promoted a significant decrease (P < 0.05) in plasma creatinine, potassium, glucose, cholesterol, low-density lipoprotein-cholesterol, triacylglycerols, uric acid and plasma renin activity, and a significant increase in plasma atrial natriuretic peptide and 24 h urinary calcium excretion. The direction of these changes did not differ between salt-sensitive and salt-resistant patients. Salt-resistant hypertensive patients exhibited a significant decrease in plasma aldosterone induced by high salt intake (from 446 ∓ 35 to 226 ± 35 pmol/l; P < 0.001), whereas this parameter was not significantly modified in salt-sensitive patients (from 485 ± 76 to 364 ± 83 pmol/l; P not significant). Salt-sensitive patients showed an increase in plasma noradrenaline after high salt intake (from 1.15 ± 0.11 to 1.56 ± 0.14 nmol/l; P < 0.05), whereas salt-resistant patients presented a decrease in this parameter (from 1.48 ± 0.08 to 1.12 ± 0.08 nmol/l; P < 0.05). The change in plasma noradrenaline was directly correlated with the change in mean blood pressure induced by high salt intake (r = 0.479; P = 0.003). 4. We conclude that the increase in blood pressure induced by high salt intake in salt-sensitive patients is associated with a stimulation of the sympathetic nervous system and a blunted decrease in plasma aldosterone. Conversely, changes in renal function, electrolyte excretion and plasma concentrations of atrial natriuretic peptide induced by high salt intake seem to be similar in both salt-sensitive and salt-resistant patients.

scholarly journals Active kallikrein response to changes in sodium-chloride intake in essential hypertensive patients.

1996 ◽  
Vol 7 (3) ◽  
pp. 443-453 ◽  
Author(s):  
C Ferri ◽  
C Bellini ◽  
A Carlomagno ◽  
G Desideri ◽  
A Santucci
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Intake ◽  
Hypertensive Patients ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium ◽  
Sodium Load ◽  
Atrial Natriuretic

To evaluate the behavior of active kallikrein excretion in salt-sensitive and salt-resistant hypertensive patients during changes in sodium-chloride (NaCl) intake, 61 male, nonobese, nondiabetic outpatients affected by uncomplicated essential hypertension were given a diet that contained 140 mmol NaCl per day for 2 wk. Patients then received either a low- (20 mmol NaCl/day) or a high- (320 mmol NaCl/day) sodium diet for 2 wk, according to a randomized, double-blind, cross-over protocol. Hypertensive patients were classified as salt sensitive when their diastolic blood pressure rose by at least 10 mm Hg after the high-sodium diet, and decreased by at least 10 mm Hg after the low-sodium diet, considering as baseline blood pressure values those that were taken at the end of the 140 mmol NaCl/day intake period. The remaining patients were classified as salt resistant or, when diastolic blood pressure increased by 10 mm Hg or more after low-sodium intake, as counter-regulating. Twenty-three patients were therefore classified as salt sensitive, 28 as salt resistant, and 10 as counter-regulating. The baseline active kallikrein excretion was significantly lower (P < 0.0001) in salt-sensitive (0.62 +/- 0.31 U/24 h) patients than in salt-resistant (1.39 +/- 0.44 U/24 h) and counter-regulating patients (1.27 +/- 0.38 U/24 h). Surprisingly, the kallikrein response to changes in sodium intake was similar in all subgroups, although enzyme excretion was always at the lowest level in salt-sensitive hypertensive patients. This latter group also showed the highest plasma atrial natriuretic peptide levels (28.2 +/- 8.5 fmol/mL, P < 0.0001 versus salt-resistant and counter-regulating patients), and the greatest peptide increment with sodium load (P < 0.0001 versus salt-resistant and counter-regulating patients). Counter-regulating patients showed the steepest increase in plasma renin activity (from 0.24 +/- 0.18 to 0.83 +/- 0.21 ng/L per s, P < 0.001) and decrease of plasma atrial natriuretic peptide (from 26.1 +/- 6.3 to 6.8 +/- 3.1 fmol/mL, P < 0.001) when switched from a high to a low-sodium intake. In conclusion, salt-sensitive hypertensive patients excrete less active kallikrein than do salt-resistant and counter-regulating patients, but maintain a normal enzyme response to changes in dietary sodium intake. The exaggerated response of atrial natriuretic peptide to high-sodium intake that was observed in the same patients could be compensating for an impaired renal capability to excrete a sodium load.

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

1988 ◽  
Vol 75 (3) ◽  
pp. 243-249 ◽  
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.

scholarly journals Atrial Natriuretic Peptide Gene and Plasma Pro-ANP Concentration in Patients with Primary Open-Angle Glaucoma

2008 ◽  
Vol 62 (6) ◽  
pp. 193-198
Author(s):  
Kristīne Baumane ◽  
Liāna Pliss ◽  
Guna Laganovska
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Promoter Region ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Proximal Promoter ◽  
Polymorphism Analysis ◽  
Hypertensive Patients ◽  
Peptide Gene ◽  
Atrial Natriuretic

Atrial Natriuretic Peptide Gene and Plasma Pro-ANP Concentration in Patients with Primary Open-Angle Glaucoma Atrial natriuretic peptide (ANP) appears to have a physiological role in volume and pressure homeostasis. Increased cardiac expression and synthesis of ANP suggest a possible local paracrine function in a number of tissues including the eye. Therefore, the identification of genetic markers may prove to be an important advance in the diagnosis of patients with glaucoma and hypertension. Plasma pro-ANP concentration was measured in 30 clinical patients. A significant elevated level of prehormone was observed in glaucoma patients with blood hypertension. Also, the distribution of the genotypes and alleles of the HpaII, SmaI and ScaI polymorphisms of the ANP gene was examined in 20 hypertensive patients with glaucoma and normotensive controls. The frequencies of the ANP genotypes and alleles did not differ significantly between controls and hypertensive patients. PCR-RFLP (polymerase chain reaction—restriction fragment length polymorphism) analysis shows a T2238→C transition in three hypertensive patients within the stop codon leading to the translation of ANP with an additional arginine. In the current study we also searched for any alterations in the 5' proximal promoter region of the ANP gene (-595 bp - -384 bp) in 20 glaucoma patients with hypertension using PCR-based SSCP (single-strand conformation polymorphism) analysis. No significant alterations in the 5' proximal promoter region of the ANP gene were observed among hypertensive patients. The structure of the ANP hormone encoded gene suggests potential importance in various diseases, but the regulatory function of ANP in the eye requires further investigations.

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.

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