The chloride channel/transporter Slc26a9 regulates the systemic arterial pressure and renal chloride excretion

2012 ◽  
Vol 91 (5) ◽  
pp. 561-572 ◽  
Author(s):  
Hassane Amlal ◽  
Jie Xu ◽  
Sharon Barone ◽  
Kamyar Zahedi ◽  
Manoocher Soleimani
Keyword(s):  
Arterial Pressure ◽  
Chloride Channel ◽  
Systemic Arterial Pressure ◽  
Chloride Excretion

Inhibitory actions of serotonin on glutamate release in dorsal medulla suppress systemic arterial pressure of cats

2004 ◽  
Vol 355 (1-2) ◽  
pp. 73-76 ◽  
Author(s):  
Chi-Li Gong ◽  
Yung-Tsung Chiu ◽  
Nai-Nu Lin ◽  
Shinn-Zong Lin ◽  
Fu-Chou Cheng ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Glutamate Release ◽  
Systemic Arterial Pressure ◽  
Dorsal Medulla

Nocturnal headache: systemic arterial pressure and heart rate during sleep

Cephalalgia ◽  
1983 ◽  
Vol 3 (1_suppl) ◽  
pp. 54-57 ◽  
Author(s):  
Fabio Cirignotta ◽  
Giorgio Coccagna ◽  
Tommaso Sacquegna ◽  
Emiliana Sforza ◽  
Giuseppe Lamontanara ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Rem Sleep ◽  
Continuous Monitoring ◽  
Systemic Arterial Pressure ◽  
Fréquence Cardiaque ◽  
The Awakening ◽  
Sono Stati ◽  
Autonomic Instability ◽  
Polygraphic Recording

In order to evaluate autonomic nervous system changes occurring before nocturnal headache attacks, we studied three subjects (one male, two females) suffering from chronic migraine. All three patients underwent a nocturnal polygraphic recording including continuous monitoring of systemic arterial pressure and heart rate. Two subjects showed increases and irregularities of arterial pressure before awakening with headache. These changes began during N–REM sleep and lasted during REM sleep preceding the awakening with headache. Heart rate did not change before the attacks. These findings do not support the hypothesis that autonomic instability during REM sleep represents the precipitating factor of the attacks. On a étudié avec des méthodes polygrafiques trois sujets (1 homme et deux femmes) souffrant d'hémicranie chronique avec des crises nocturnes. Chez deux malades les crises étaient précédées d'augmentation et d'irrégularité de la tension artérielle. Ces modifications commençaient pendant le sommeil N-REM et contineaient pendant le sommeil REM qui précédait le réveil avec hémicranie. La fréquence cardiaque n'a pas subi de modification avant les crises. Les résultats obtenus ne confirment l'hypothèse selon laquelle le facteur causant les crises est l'instabilité anticronique à la fase REM. Sono stati studiati con metodiche poligrafiche 3 soggetti (1 maschio e 2 femmine) affetti da emicrania cronica con attacchi notturni. In 2 di essi gli attacchi erano preceduti da incrementi ed irregolarità della pressione arteriosa. Tali modificazioni iniziavano durante il sonno N-REM e perduravano nel corso del sonno REM che precedeva il risveglio con cefalea. La frequenza cardiaca non si modificava prima dell'attacco. I risultati ottenuti non confermano l'ipotesi che il fattore precipitante gli attacchi emicranici sia l'instabilità anticronica della fase REM.

Chronic EDRF inhibition and hypoxia: effects on pulmonary circulation and systemic blood pressure

1993 ◽  
Vol 75 (4) ◽  
pp. 1748-1757 ◽  
Author(s):  
V. Hampl ◽  
S. L. Archer ◽  
D. P. Nelson ◽  
E. K. Weir
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Systemic Blood Pressure ◽  
Systemic Circulation ◽  
Systemic Arterial Pressure ◽  
Hypoxic Pulmonary Hypertension ◽  
Basal Tone ◽  
Isolated Lungs

It has been suggested that chronic hypoxic pulmonary hypertension results from chronic hypoxic inhibition of endothelium-derived relaxing factor (EDRF) synthesis. We tested this hypothesis by studying whether chronic EDRF inhibition by N omega-nitro-L-arginine methyl ester (L-NAME) would induce pulmonary hypertension similar to that found in chronic hypoxia. L-NAME (1.85 mM) was given for 3 wk in drinking water to rats living in normoxia or hypoxia. Unlike chronic hypoxia, chronic L-NAME treatment did not increase pulmonary arterial pressure. Cardiac output was reduced and mean systemic arterial pressure was increased by chronic L-NAME treatment. The vascular pressure-flow relationship in isolated lungs was shifted toward higher pressures by chronic hypoxia and, to a lesser degree, by L-NAME intake. In isolated lungs, vasoconstriction in response to angiotensin II and acute hypoxia and vasodilation in response to sodium nitroprusside were increased by chronic L-NAME treatment in normoxia and chronic hypoxia. Chronic hypoxia, but not L-NAME, induced hypertensive pulmonary vascular remodeling. Chronic supplementation with the EDRF precursor L-arginine did not have any significant effect on chronic hypoxic pulmonary hypertension. We conclude that the chronic EDRF deficiency state, induced by L-NAME, does not mimic chronic hypoxic pulmonary hypertension in our model. In addition, EDRF proved to be less important for basal tone regulation in the pulmonary than in the systemic circulation.

Mechanisms of centrally administered ET-1-induced increases in systemic arterial pressure and AVP secretion

1997 ◽  
Vol 272 (1) ◽  
pp. E126-E132 ◽  
Author(s):  
N. F. Rossi ◽  
D. S. O'Leary ◽  
H. Chen
Keyword(s):  
Arterial Pressure ◽  
Peak Plasma ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Fold Increase ◽  
Systemic Arterial Pressure ◽  
Sympathetic Outflow ◽  
Central Administration ◽  
Eta Receptor ◽  
The Central Nervous System

Endothelins (ET) within the central nervous system (CNS) alter systemic cardiovascular responses and arginine vasopressin (AVP) secretion. These experiments were designed to ascertain whether the rise in systemic arterial pressure after central administration of ET-1 is mediated by enhancing sympathetic outflow and/or circulating AVP. In Long-Evans (LE/LE) rats, intracerebroventricular injection of 1-10 pmol ET-1 dose dependently increased mean arterial pressure (MAP). Peak response occurred 7-12 min after ET-1 and was inhibited by ETA receptor antagonism. Systemic vasopressin (V1) receptor blockade did not inhibit the pressor response, and rats with central diabetes insipidus (DI/DI) displayed an identical rise in MAP. Ganglionic blockade prevented ET-1-induced hemodynamic effects. Peak plasma AVP levels occurred 60 min after ET-1, as the pressor response began to wane. In sinoaortic-denervated LE/LE rats, ET-1 elicited a 10-fold increase in AVP secretion that coincided with the hemodynamic changes and was blocked by BQ-123. Thus ET-1 via ETA receptors within the CNS induced a concentration-dependent increase in systemic arterial pressure mediated by enhanced sympathetic outflow but not by circulating AVP. Reflex baroreceptor activation attenuated AVP release.

New analytic framework for understanding sympathetic baroreflex control of arterial pressure

1999 ◽  
Vol 276 (6) ◽  
pp. H2251-H2261 ◽  
Author(s):  
Takayuki Sato ◽  
Toru Kawada ◽  
Masashi Inagaki ◽  
Toshiaki Shishido ◽  
Hiroshi Takaki ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Equilibrium Diagram ◽  
Feedback System ◽  
Systemic Arterial Pressure ◽  
Equation Model ◽  
Operating Point ◽  
Baroreflex Control ◽  
Efferent Nerve ◽  
Severe Hemorrhage ◽  
Mean Square Errors

The sympathetic baroreflex is an important feedback system in stabilization of arterial pressure. This system can be decomposed into the controlling element (mechanoneural arc) and the controlled element (neuromechanical arc). We hypothesized that the intersection of the two operational curves representing their respective functions on an equilibrium diagram should define the operating point of the arterial baroreflex. Both carotid sinuses were isolated in 16 halothane-anesthetized rats. The vagi and aortic depressor nerves were cut bilaterally. Carotid sinus pressure (CSP) was sequentially altered in 10-mmHg increments from 80 to 160 mmHg while sympathetic efferent nerve activity (SNA) and systemic arterial pressure (SAP) were recorded simultaneously under various hemorrhagic conditions. The mechanoneural arc was characterized by the response of SNA to CSP and the neuromechanical arc by the response of SAP to SNA. We parametrically analyzed the relationship between input and output for each arc using a four-parameter logistic equation model. In baseline states, the two arcs intersected each other at the point at which the instantaneous gain of each arc attained its maximum. Severe hemorrhage lowered the gain and offset of the neuromechanical arc and moved the operating point, whereas the mechanoneural arc remained unchanged. The operating points measured under the closed-loop conditions were indistinguishable from those estimated from the intersections of the two arc curves on the equilibrium diagram. The average root mean square errors of estimate for arterial pressure and SNA were 2 and 3%, respectively. Such an analytic approach could explain a mechanism for the determination of the operating point of the sympathetic baroreflex system and thus helps us integratively understand its function.

Rebound cardiovascular responses following stimulation of canine vagosympathetic complexes or cardiopulmonary nerves

1985 ◽  
Vol 63 (9) ◽  
pp. 1122-1132 ◽  
Author(s):  
J. A. Armour ◽  
W. C. Randall
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Cardiac Responses ◽  
Stimulation Of

Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.

Effect of Sustained-Release Verapamil on the Morning Systemic Arterial Pressure Surge During Daily Activity in Patients With Systemic Hypertension

1997 ◽  
Vol 79 (9) ◽  
pp. 1252-1255 ◽  
Author(s):  
Guido A Rosito ◽  
Otavio C.E Gebara ◽  
Carol A McKenna ◽  
Harold S Solomon ◽  
James E Muller ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sustained Release ◽  
Daily Activity ◽  
Systemic Arterial Pressure ◽  
Systemic Hypertension ◽  
Sustained Release Verapamil ◽  
Pressure Surge
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