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  • 1
    ISSN: 1432-2013
    Keywords: Blood pressure ; Kidney blood flow ; Autoregulation ; Renin release ; Pressoreceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 1. The effect of varying renal artery pressure between 160 and 40 mm Hg on renal blood flow and renin release was studied in seven conscious foxhounds under β-adrenergic blockade receiving a normal sodium diet (4.1 mmol/kg/day). Pressure was either increased by bilateral common carotid occlusion or reduced in steps and maintained constant by a control-system using an inflatable renal artery cuff. Carotid occlusion itself had no influence on renal blood flow and renin release when renal artery pressure was kept constant and the β-receptors in the kidney were blocked. 2. Between 160 mm Hg and resting pressure there was no change in renal blood flow; between resting blood pressure and the lower limit of autoregulation (average 63.9 mm Hg) renal blood flow increased slightly (average 7%) indicating a high efficiency of renal blood flow autoregulation. 3. The relationship between renal artery pressure and renin release could be approximated by two linear sections:a low sensitivity to a pressure change (average slope: −0.69 ±0.26ng AI/min/mm Hg) was found above a threshold pressure (average: 89.8±3.3 mm Hg) and a high sensitivity to a pressure change (average slope: −64.4±20.8 ng AI/ min/mm Hg) was observed between threshold pressure and 60 mm Hg. There was no further increase of renin release between 60 and 40 mm Hg. 4. It is concluded that within the autoregulatory plateau the kidney of a conscious β-blocked dog receiving a normal sodium diet releases only negligible amounts of renin until renal artery pressure falls below a threshold pressure of 90 mm Hg which is close to the animals resting systemic pressure. Since beyond that a decrease of systemic pressure by as little as 1.3 mm Hg below threshold can raise resting renin release (84.8±29.8 ng/min) by 100%, it is suggested that systemic blood pressure tends to stabilize at a level at which renin release is minimal.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 327 (1971), S. 203-224 
    ISSN: 1432-2013
    Keywords: Pressoreceptors ; Cardiac Output ; Blood Pressure ; Autoregulation ; Sympatholytics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Flow velocity in the ascending aorta and aortic blood pressure were recorded continuously in healthy conscious dogs. Using implanted pneumatic cuffs the effect of bilateral carotid occlusion on heart rate, stroke volume, cardiac output, peak velocity, maximum acceleration, blood pressure, and total peripheral resistance (T.P.R.) was studied in the resting animal. Following carotid occlusion heart rate rose within 3–4 sec by 13 beats/min; during the steady state it exceeded the control by 8 beats/min. Cardiac output closely followed heart rate, since stroke volume decreased slightly (3–4%), mainly because of the elevated aortic pressure. During the first 3–4 sec cardiac output increased by 10–15% reaching a steady state level 8% above control. The initial fast increase of cardiac output caused mean aortic pressure to rise rapidly, while T.P.R. transiently decreased. Subsequently T.P.R. rose, causing a secondary slow increase of pressure. During the steady state blood pressure was elevated by 27 mm Hg (26%), T.P.R. by 12.1 mm Hg×l−1×min (20%). Maximum acceleration did not change with heart rate and was hardly affected (−1.5%) by the pressure rise. Peak velocity was little influenced by heart rate; it decreased by 7% mainly because of the elevated aortic pressure. β-blockade (0.5 mg/kg propranolol) affected T.P.R. only during control (+18%), but did not modify the time course of the reflex and its steady state changes. α-blockade (5.0 mg/kg phenoxybenzamine) decreased aortic mean pressure (5 mm Hg) and T.P.R. (7%) during control. Following carotid occlusion T.P.R. rose by the same amount, but much more slowly. Starting from the lower control the same pressure level was now obtained by a higher reflex increase of heart rate and cardiac output. It is concluded that the initial pressor response is initiated by an increase of cardiac output mediated by vagal inhibition. The secondary rise of blood pressure is predominantly caused by an increase of T.P.R. due to autoregulation in some vascular beds. The higher stroke work during the reflex is not accomplished by an increased contractility due to sympathetic activation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 337 (1972), S. 59-70 
    ISSN: 1432-2013
    Keywords: Pressoreceptors ; Parasympatholytics ; Pacemaker, Artificial ; Cardiac Output ; Vascular Resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In healty, conscious dogs the heart rate was kept constant at 144 to 146 beats per minute either by vagal blockade with Atropine (0,5 mg/kg i.v.) or by electrical pacing of the heart. In the resting dog a carotid-sinus-reflex was elicited clamping both common carotid arteries with implanted pneumatic cuffs. Velocity in the ascending aorta (electromagnetic flowmeter), pressure in the descending thoracic aorta (implanted miniature pressure transducer) and pressure in the right carotid sinus using a catheter were measured. By analogue processing acceleration in the ascending aorta, stroke volume and stroke work of the left ventricle, and mean values were derived. Compared to the reflex under normal resting heart rates (64 beats per minute) the results show, that with a constant heart rate (144–146 beats per minute) blood pressure rises by about the same amount induced by a larger increase of the peripheral resistance. Because the fast increase of cardiac output regularly observed under normal conditions was eliminated, the time course of pressure elevation was slower when heart rate was kept constant. The elevated stroke work of the left ventricle during carotid occlusion cannot be explained by an increase of contractility due to enhanced sympathetic activity, because no such increase in contractility was found. It is suggested, that a low control heart rate allows fast reflex adjustment of blood pressure mediated by increases of cardiac output due to vagal inhibition. In contrast, when heart rate is high due to vagal blockade or electrical pacing, the reflex response is determined by slow changes of the total peripheral resistance.
    Type of Medium: Electronic Resource
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