Control of respiratory and hypotensive response during hypoxic chemoreflex by A5 region neurons in rats

2006 ◽  
Vol 142 (6) ◽  
pp. 654-656 ◽  
Author(s):  
V. F. Pyatin ◽  
V. S. Tatarnikov ◽  
E. N. Glazkova
1971 ◽  
Vol 72 (5) ◽  
pp. 923-925 ◽  
Author(s):  
Laurence S. Harris ◽  
Miles A. Galin
Keyword(s):  

1978 ◽  
Vol 55 (s4) ◽  
pp. 65s-68s ◽  
Author(s):  
D. Cousineau ◽  
J. de Champlain ◽  
L. Lapointe

1. Average supine circulating total catecholamine concentrations were found to be higher than the normal range in about 50% of patients with labile hypertension and in about 30% of patients with sustained essential hypertension. 2. These higher resting concentrations were mainly due to an increase in adrenaline in labile hypertension and to an increase in noradrenaline in sustained hypertension. 3. Patients with elevated catecholamine concentrations were also characterized by a higher heart rate, by an increased myocardial contractility and by greater hypotensive response after treatment with β-adrenoreceptor blocking agents. 4. These studies suggest the existence of subgroups of hypertensive patients with increased sympathetic tone.


1989 ◽  
Vol 257 (2) ◽  
pp. H611-H617 ◽  
Author(s):  
S. R. Reddy ◽  
R. Talwalkar ◽  
J. Downs ◽  
T. A. Kotchen

High dietary intake of linoleic acid lowers arterial pressure, and, in vitro, linoleic acid inhibits the enzymatic activity of renin. The purpose of the present study was 1) to evaluate the effect of intravenous infusion of linoleic acid on blood pressure in normotensive and hypertensive Sprague-Dawley rats and 2) to determine whether the hypotensive response to linoleic acid infusion is caused by inhibition of circulating renin. Blood pressure was decreased (P less than 0.01) by linoleic acid infusion in normotensive sodium chloride-deprived animals and in animals with two-kidney, one-clip hypertension. In contrast, linoleic acid infusion did not affect blood pressure in normotensive rats on a "normal" or high sodium chloride intake, in rats with deoxycorticosterone acetate (DOCA)-salt hypertension, and in anephric rats. In sodium chloride-deprived rats, the reduction of blood pressure by linoleic acid infusion was associated with increased plasma renin activity (P less than 0.05); serum angiotensin-converting enzyme activity was unchanged. The in vitro enzymatic activity of exogenous renin in plasma of anephric rats was not affected by linoleic acid infusion. In two-kidney, one-clip hypertensive animals, pretreatment with indomethacin did not alter the hypotensive response to linoleic acid. Thus, although linoleic acid infusion lowered blood pressure in high renin but not in low renin states, the reduction of blood pressure was not related to inhibition of circulating renin or to alterations of endogenous prostaglandin biosynthesis.


1993 ◽  
Vol 264 (1) ◽  
pp. R73-R78 ◽  
Author(s):  
E. Mills ◽  
C. M. Kuhn ◽  
M. N. Feinglos ◽  
R. Surwit

The C57BL/6J (BL/6) mouse develops non-insulin-dependent diabetes mellitus (NIDDM) when fed a high fat-high simple carbohydrate (HFHSC) diet, whereas A/J mice do not. The purpose of the study was to determine whether hypertension occurred with NIDDM and whether it was sustained by sympathetic nervous system (SNS) hyperactivity. After 3 mo on an HFHSC diet with a low Na content (0.06%), awake, tail-cuff systolic blood pressure (BP) increased 20% above the control diet in BL/6 (138 +/- 3 vs. 115 +/- 4) but not in A/J (115 +/- 6 vs. 113 +/- 2 mmHg) mice. On a normal Na (0.4%)-HFHSC diet, BL/6 mice had a higher BP than on 0.06% Na (149 +/- 3 at 3 mo, 162 +/- 6 at 4.5 mo). After 1 mo on the 0.06% Na-HFHSC diet, direct BP of anesthetized BL/6 mice was 18% higher than control. The hypotensive response to interruption of SNS activity by ganglionic blockade (chlorisondamine) increased in the BL/6 mice (50%), whereas the heart rate response increased in both strains (20-30%). Analysis of variance (ANOVA) on glucose detected significant effects of strain and diet and a strain x diet interaction (P = 0.0007). At 1 or 3 mo, HFHSC-fed BL/6 mice were hyperglycemic (> 11 mM) compared with diet or strain controls. The ANOVA on insulin detected strain and diet effects but not a strain x diet interaction (P = 0.3). HFHSC increased insulin above the control of 140-160 pM in A/J and BL/6 strain (20-70% at 1 mo, 400% at 3 mo).(ABSTRACT TRUNCATED AT 250 WORDS)


2013 ◽  
Vol 98 (8) ◽  
pp. 1279-1294 ◽  
Author(s):  
M. V. López-González ◽  
A. Díaz-Casares ◽  
C. A. Peinado-Aragonés ◽  
J. P. Lara ◽  
M. A. Barbancho ◽  
...  

2008 ◽  
pp. 137-139
Author(s):  
S Čačányiová ◽  
F Kristek ◽  
J Kuneš ◽  
J Zicha

We investigated the effect of pertussis toxin (PTX) on hypotensive response induced by acetylcholine (ACh) and bradykinin (BK) and on noradrenaline (NA)-induced pressor response in spontaneously hypertensive rats (SHR). Fifteenweek-old Wistar rats and age-matched SHR were used. Half of SHR received PTX (10 µg/kg/i.v.) and the experiments were performed 48 h later. After the anesthesia the right carotid artery was cannulated in order to record blood pressure (BP). The hypotensive response to ACh was enhanced in SHR compared to Wistar rats. After pretreatment of SHR with PTX the hypotensive response to ACh was reduced compared to untreated SHR and it was also diminished in comparison to Wistar rats. Similarly, the hypotensive response to BK was also decreased after PTX pretreatment. The pressor response to NA was increased in SHR compared to Wistar rats. NA-induced pressor response was considerably decreased after PTX pretreatment compared to untreated SHR. In conclusion, the enhancement of hypotensive and pressor responses in SHR was abolished after PTX pretreatment. Our results suggested that the activation of PTXsensitive inhibitory Gi proteins is involved in the regulation of integrated vasoactive responses in SHR and PTX pretreatment could be effectively used for modification of BP regulation in this type of experimental hypertension.


Hypertension ◽  
1987 ◽  
Vol 10 (3) ◽  
pp. 254-258 ◽  
Author(s):  
L M Resnick ◽  
J P Nicholson ◽  
J H Laragh
Keyword(s):  

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