scholarly journals Increased arterial blood pressure and volume expansion in Atrap (angiotensin receptor‐associated protein) – deficient mice

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Mona Oppermann ◽  
Hayo Castrop
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Volume Expansion ◽  
Angiotensin Receptor ◽  
Receptor Associated Protein ◽  
Arterial Blood ◽  
Deficient Mice

Blood volume changes and high and low pressoreceptor activity in cats

1984 ◽  
Vol 247 (5) ◽  
pp. R833-R836 ◽  
Author(s):  
E. Tomomatsu ◽  
J. P. Gilmore
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Mean Arterial Blood Pressure ◽  
Volume Expansion ◽  
Carotid Sinus ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Blood Volume Expansion ◽  
Aortic Baroreceptors

Studies were undertaken in the cat to determine if moderate hemorrhage or volume expansion significantly altered carotid sinus and aortic baroreceptor activity. In addition, the experimental design provided the opportunity to compare gain of the two sets of receptors. A 20% blood volume expansion increased mean arterial blood pressure 5.2% and carotid sinus nerve activity 14.7%, whereas a 20% hemorrhage decreased mean arterial blood pressure 10.8% and carotid sinus nerve activity 32.3%. For the aortic baroreceptors, a 20% blood volume expansion increased mean arterial blood pressure 5.9% and nerve activity 10.5%, and a 20% hemorrhage decreased mean arterial blood pressure 8.9% and nerve activity 21.0%. The blood pressure-discharge curves for the carotid sinus and aortic baroreceptors were not different. The well-known high sensitivity of atrial receptors was also documented. We conclude that both high- and low-pressure receptors apprise the central nervous system of the status of intravascular volume and pressure.

Exaggerated natriuresis during clamping of systemic NO supply in healthy young men

2011 ◽  
Vol 122 (2) ◽  
pp. 63-73 ◽  
Author(s):  
Jane A. Simonsen ◽  
Mona S. Rasmussen ◽  
Werner Vach ◽  
Poul F. Høilund-Carlsen ◽  
Peter Bie
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Peripheral Resistance ◽  
Young Men ◽  
System Activity ◽  
Arterial Blood

NO (nitric oxide) may be involved in fluid homoeostasis. We hypothesized that increases in NO synthesis contribute to acute, saline-induced natriuresis, which, therefore, should be blunted when NO availability is stabilized. Young men were studied during simultaneous infusions of L-NAME [NG-nitro-L-arginine methyl ester; bolus of 750 μg·kg−1 of body weight and 8.3 μg·min−1·kg−1 of body weight] and SNP (sodium nitroprusside), the latter at a rate preventing L-NAME from increasing total peripheral resistance (‘NO-clamping’). Slow volume expansion (saline, 20 μmol of NaCl·min−1·kg−1 of body weight for 3 h) was performed with and without concomitant NO-clamping. NO-clamping itself decreased RPF (renal plasma flow; P~0.02) and tended to decrease arterial blood pressure [MABP (mean arterial blood pressure)]. Volume expansion markedly decreased the plasma levels of renin, AngII (angiotensin II) and aldosterone (all P<0.001), while MABP (oscillometry), heart rate, cardiac output (impedance cardiography), RPF (by p-aminohippurate), GFR [glomerular filtration rate; by using 51Cr-labelled EDTA] and plasma [Na+] and [K+] remained constant. Volume expansion increased sodium excretion (P<0.02) at constant filtered load, but more so during NO-clamping than during control (+184% compared with 52%; P<0.0001). Urinary nitrate/nitrite excretion increased during volume expansion; plasma cGMP and plasma vasopressin were unchanged. The results demonstrate that NO-clamping augments sodium excretion in response to volume expansion at constant MABP and GFR, reduced RPF and decreased renin system activity, a response termed hypernatriuresis. The results indicate that mediator(s) other than MABP, RPF, GFR and renin system activity contribute significantly to the homoeostatic response to saline loading, but the specific mechanisms of hypernatriuresis remain obscure.

Autonomic nervous system and blood pressure regulation in RGS2-deficient mice

2005 ◽  
Vol 288 (5) ◽  
pp. R1134-R1142 ◽  
Author(s):  
Volkmar Gross ◽  
Jens Tank ◽  
Michael Obst ◽  
Ralph Plehm ◽  
Kendall J. Blumer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Environmental Stress ◽  
G Protein ◽  
Arterial Blood Pressure ◽  
Stress Sensitivity ◽  
Pressure Regulation ◽  
Arterial Blood ◽  
Deficient Mice

Regulator of G protein signaling (RGS2) deletion in mice prolongs signaling by G protein-coupled vasoconstrictor receptors and increases blood pressure. However, the exact mechanism of the increase in blood pressure is unknown. To address this question we tested autonomic nervous system function and blood pressure regulation in RGS2-deficient mice (RGS2 −/−). We measured arterial blood pressure and heart rate (HR) with telemetry, computed time and frequency-domain measures for blood pressure and HR variability (HRV) as well as baroreflex sensitivity [BRS-low frequency (LF)], and assessed environmental stress sensitivity. Mean arterial blood pressure (MAP) was ∼10 mmHg higher in RGS2 −/− compared with RGS2 +/+ mice, while HR was not different between the groups, indicating a resetting of the baroreceptor reflex. Atropine increased MAP more in RGS2 −/− than in RGS2 +/+ mice while HR responses were not different. Urinary norepinephrine excretion was higher in RGS2 −/− than in RGS2 +/+ mice. The blood pressure decrease following prazosin was more pronounced in RGS2 −/− mice than in RGS2 +/+ mice. The LF and high-frequency (HF) power of HRV were reduced in RGS2 −/− compared with controls while BRS-LF and SBP-LF were not different. Atropine and atropine + metoprolol markedly reduced the HRV parameters in the time (RMSSD) and frequency domain (LF, HF, LF/HF) in both strains. Environmental stress sensitivity was increased in RGS2 −/− mice compared with controls. We conclude that the increase in blood pressure in RGS2 −/− mice is not solely explained by peripheral vascular mechanisms. A central nervous system mechanism might be implicated by an increased sympathetic tone. This state of affairs could lead to a baroreceptor-HR reflex resetting, while BRS remains unimpaired.

scholarly journals Raised arterial blood pressure in neurokinin-1 receptor-deficient mice (NK1R−/−): evidence for a neural rather than a vascular mechanism

2016 ◽  
Vol 101 (5) ◽  
pp. 588-598 ◽  
Author(s):  
Amie J. Moyes ◽  
S. Clare Stanford ◽  
Patrick S. Hosford ◽  
Adrian J. Hobbs ◽  
Andrew G. Ramage
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Neurokinin 1 Receptor ◽  
Arterial Blood ◽  
Neurokinin 1 ◽  
Deficient Mice
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