Hypertension Induced by Prolonged Intracoronary Administration of Dobutamine in Conscious Dogs

1978 ◽  
Vol 54 (2) ◽  
pp. 153-160 ◽  
Author(s):  
J.-F. Liard
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Electromagnetic Flowmeter ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Control Value ◽  
A Value

1. In order to determine if a sustained increase in cardiac output can lead to hypertension, seven conscious dogs were given a continuous infusion of dobutamine, a powerful stimulant of cardiac inotropism, into the left coronary artery for a 7 day period while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured. 2. The infusion technique (1·5 × 10−8 mol min−1 kg−1, intracoronary) was selected after short-term experiments showed that it increased cardiac output more effectively than intravenous infusion at the same rate. 3. The rise in cardiac output elicited by intracoronary infusion of dobutamine was largest during the first 6 h of the 7 days administration, at which time calculated peripheral resistance was decreased. Subsequently, cardiac output returned progressively toward its control value whereas mean arterial pressure remained elevated (by an average of 20–25 mmHg) and peripheral resistance increased significantly. 4. Measurements of blood and extracellular fluid volumes as well as plasma renin activity indicated that these factors were not involved in the blood pressure increase. 5. When the infusion was ended, arterial pressure fell rapidly but peripheral resistance remained elevated during the first 6 h. Cardiac output fell after 2 and 6 h to a value below that of the pre-infusion control. After 1 day and subsequently, blood pressure became normal, as did the peripheral resistance and cardiac output. 6. Both at the onset and offset transients of this model of hypertension, changes in cardiac output preceded changes in peripheral resistance. These experiments may give experimental support to the concept of cardiogenic hypertension.

Pathogenesis of Arterial Hypertension after the Constriction of the Renal Artery Leaving the opposite Kidney Intact Both in the Anaesthetized and in the Conscious Dog

1972 ◽  
Vol 42 (6) ◽  
pp. 651-664 ◽  
Author(s):  
G. Bianchi ◽  
E. Baldoli ◽  
R. Lucca ◽  
P. Barbin
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Plasma Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Plasma Renin Concentration ◽  
Renal Artery Constriction

1. The renal artery was constricted leaving the opposite kidney intact in ten conscious and seven anaesthetized dogs. Intravenous infusion of exogenous renin was done in seven conscious dogs; in four of these the renal artery was constricted 15–17 days later. The following variables were measured in all animals before and after renal artery constriction: plasma renin concentration, blood pressure, cumulative sodium balance, plasma volume, extracellular fluid volume and plasma non-protein nitrogen. Before and after renal artery constriction in the conscious dogs cardiac output, stroke volume, total peripheral resistance and cardiac rate were also measured. In a few dogs angiotensin responsiveness and plasma concentration of renin substrate were also measured. 2. There was no significant difference between the regression of change in blood pressure on change in plasma renin concentration within 2 h from renal artery constriction in the conscious dogs and that observed during intravenous infusion of renin. Comparing the changes of these variables with the ones previously obtained with renal artery constriction to the lone remaining kidney, for a given increase of plasma renin concentration the rise of blood pressure was lower when the contralateral kidney was untouched. The changes of the other variables in the conscious dogs may be divided into three phases: a first phase lasting hours, in which, besides the changes described above, there was an increase of total peripheral resistance while the other variables remain unchanged: a second phase, 24 h after constriction, in which blood pressure, total peripheral resistance and plasma renin clearance decreased while plasma volume, cardiac output and extracellular fluid volume slightly increased; however, only the plasma volume change was statistically significant: and a third phase 6–7 days after constriction, when all the variables returned towards normal values, except that the blood pressure and total peripheral resistance remained significantly higher. Sodium balance remained at equilibrium throughout the study period. It is suggested that these results are compatible with the ‘autoregulation theory’ of renal hypertension. 3. Renal artery constriction in the anaesthetized animals caused a slight but significant sodium retention that very likely influenced the sequence of the events. On the second day after constriction, the plasma renin concentration was significantly increased, whereas the highest values of blood pressure, plasma volume and extracellular fluid volume occurred on the seventh day after constriction.

Cardiogenic Hypertension: Experimental Evidence from a Comparison between Intravenous and Intracoronary Administration of Dobutamine in Conscious Dogs

1980 ◽  
Vol 58 (4) ◽  
pp. 271-277 ◽  
Author(s):  
J.-F. Liard
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Conscious Dogs ◽  
Cardiac Effects ◽  
Intracoronary Administration ◽  
Haemodynamic Changes ◽  
Propranolol Treatment ◽  
Oral Propranolol

1. We have studied whether the progressive rise in peripheral resistance observed in response to chronic intracoronary administration of dobutamine in conscious dogs could have resulted from extracardiac or non-β-adrenergic cardiac effects of the drug. 2. Six conscious dogs received dobutamine, 1.56 × 10−8 mol min−1 kg−1, intravenously for a 7 day period and seven conscious dogs were given dobutamine, 1.51 × 10−8 mol min−1 kg−1, into the left coronary artery under oral propranolol treatment for the same period while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured. 3. Intravenous dobutamine produced no increase in arterial pressure, but a decrease in peripheral resistance and an increase in cardiac output which persisted until the end of the infusion. 4. With propranolol treatment intracoronary dobutamine induced no significant haemodynamic changes but a short-lasting increase in mean arterial pressure and peripheral resistance. 5. It is concluded that β-adrenergic cardiac effects of dobutamine are essential to the development of hypertension and increased peripheral resistance after prolonged intracoronary infusion of this drug.

V1 vs. combined V1+V2 vasopressin blockade after hemorrhage in conscious dogs

1988 ◽  
Vol 255 (6) ◽  
pp. H1325-H1329
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Conscious Dogs ◽  
Hemodynamic Changes ◽  
Significant Difference ◽  
V2 Antagonist

We examined the hypothesis that V2-like receptors might contribute to the hemodynamic response seen after blockade of the vasoconstrictor (V1) effect of arginine vasopressin (AVP) in nonhypotensive hemorrhage. Seven chronically instrumented dogs were bled 15 ml/kg within 15 min on two different days, at least 3 days apart, and then injected either with the V1 antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)2-(O-methyl)tyrosine]AVP [d(CH2)5Tyr(Me)AVP, 10 micrograms/kg] or with the combined V1+V2 antagonist [1(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)2-(O-ethyl)-D-tyrosine)4-valine]AVP [d(CH2)5-D-Tyr-(Et)VAVP (10 micrograms/kg)]. Mean arterial pressure, heart rate, and cardiac output (electromagnetic flowmeter) were measured before as well as after hemorrhage and for 10 min after antagonist administration. Both antagonists given after hemorrhage significantly decreased mean arterial pressure as well as total peripheral resistance and increased cardiac output. The V1 antagonist also increased heart rate significantly. No significant hemodynamic changes were measured in another group of six dogs in the absence of antagonist treatment. Although hemodynamic changes tended to be greater with the V1 antagonist than with the combined V1+V2 antagonist, a significant difference between the two analogues was established only for heart rate. These results indicate that in hemorrhage interaction with V2-like receptors plays only a modest role in the hemodynamic changes after V1 blockade in conscious dogs, contrary to what was found in dehydration.

Effects of phenoxybenzamine, metoprolol, captopril, and meclofenamate on cardiovascular function in deoxycorticosterone acetate hypertensive Yucatan miniature swine

1983 ◽  
Vol 61 (2) ◽  
pp. 149-153 ◽  
Author(s):  
Charles D. Ciccone ◽  
Edward J. Zambraski
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Response Curves ◽  
Miniature Swine ◽  
Deoxycorticosterone Acetate ◽  
Adrenergic Activity ◽  
Conscious Animals

Eight adult Yucatan miniature swine were implanted with deoxycorticosterone acetate (DOCA) impregnated silicone strips (100 mg∙kg−1). After 16 weeks of DOCA treatment mean arterial pressure (MAP) increased to 183 ± 4 mmHg (1 mmHg = 133.322 Pa). In four normal animals arterial pressure was 126 ± 8 mmHg. The increase in MAP in the DOCA animalas was due to an elevated total peripheral resistance (TPR) with cardiac output remaining normal. In tests with conscious animals, phenoxybenzamine (1 mg∙kg−1) significantly decreased arterial pressure via a selective decrease in TPR. Neither meclofenamate, metoprolol, nor captopril affected MAP in these DOCA hypertensive animals. Dose–response curves to exogenous norepinephrine and angiotensin II revealed that the DOCA animals had an increased pressor sensitivity to both of these agents. These data suggest that in the DOCA hypertensive Yucatan swine an increase in alpha adrenergic activity and (or) an increase in smooth muscle responsiveness to circulating catecholamines is responsible for the increase in blood pressure as a result of an increase in total peripheral resistance.

Plasma Renin Levels and Systemic Haemodynamics in Essential Hypertension

1977 ◽  
Vol 52 (6) ◽  
pp. 591-597 ◽  
Author(s):  
R. Fagard ◽  
A. Amery ◽  
T. Reybrouck ◽  
P. Lijnen ◽  
L. Billiet ◽  
...  
Keyword(s):  
Renal Function ◽  
Cardiac Output ◽  
Essential Hypertension ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Inverse Relation ◽  
Plasma Renin Concentration ◽  
Low Renin Hypertension

1. Plasma renin concentration, intra-arterial pressure, cardiac output and total peripheral resistance have been studied in 50 patients with essential hypertension and normal renal function. 2. Total peripheral resistance and plasma renin were negatively correlated (r = −0·45), indicating that ‘high-renin’ essential hypertension is not necessarily associated with arteriolar vasoconstriction. 3. The inverse relation between mean arterial pressure and plasma renin (r = −0·46) suggests a role for the renal baroreceptor mechanism in the suppression of renin in ‘low-renin’ hypertension. 4. Cardiac output was positively related to plasma renin concentration (r = +0·42). 5. Multiple regression analysis indicates that the described relationships were independent of age.

Contribution of Stenosis Resistance to the Rise in total Peripheral Resistance during Experimental Renal Hypertension in Conscious Dogs

1981 ◽  
Vol 61 (6) ◽  
pp. 663-670 ◽  
Author(s):  
W. P. Anderson ◽  
P. I. Korner ◽  
J. A. Angus ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Plasma Renin Activity ◽  
Renal Artery ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Vascular Beds ◽  
Renal Vascular

1. Mild, moderate and severe renal artery stenosis was induced in uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, followed by a return to control values 24 h after cuff deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. in moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. in these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. in mild stenosis the changes in both cardiac output and total peripheral resistance were variable and not statistically significant. in this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. in all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of nonrenal beds.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

Long-term hypotensive effect of beta-agonist in conscious dogs

1988 ◽  
Vol 255 (3) ◽  
pp. H592-H600
Author(s):  
B. S. Nuwayhid ◽  
D. B. Young ◽  
U. Tipayamontri ◽  
J. P. Montani
Keyword(s):  
Renal Function ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Hypotensive Effect ◽  
Beta Agonist ◽  
Plasma Protein Concentration ◽  
Conscious Animal

The purpose of this study was to investigate the arterial pressure response to long-term administration of beta-agonists in the chronically instrumented conscious animal model. Chronically instrumented dogs were given intravenous infusions of ritodrine (2 micrograms.kg-1.min-1) for a period of 2 wk. Several cardiovascular and renal parameters were monitored before, during, and after the ritodrine infusion, and renal function curves were constructed. After the 1st wk of infusion, a new steady state was reestablished, and this was characterized by hypotension, reduced plasma protein concentration, elevated cardiac output, expanded extracellular fluid space, and near normal levels of activity of renin-angiotensin-aldosterone systems. The renal function curve during ritodrine infusion shifted to the left with no change in slope. We propose the following: 1) the persistence of hypotension is most probably related to the resetting of the arterial pressure-kidney blood volume servocontrol mechanisms, and 2) the persistent elevation of cardiac output and reduction in peripheral resistance are most probably related to increased oxygen and nutrient demand during beta-agonist infusions.

Haemodynamic Profile of Angiotensin II Antagonism in Essential Hypertensive Patients

1979 ◽  
Vol 57 (s5) ◽  
pp. 119s-121s
Author(s):  
S. N. Hunyor ◽  
H. Larkin ◽  
Janet Rowe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Heart Rate Effect

1. The haemodynamic response to antagonistic (10 μg min−1 kg−1) and agonistic (40 μg min−1 kg−1) doses of saralasin was studied in young essential hypertensive patients. Blood pressure behaviour alone was thought to be inadequate to describe the response pattern. 2. Pre-saralasin setting of the renin-angiotensin axis was varied with salt intake (15 and 290 mmol of Na+/day) each for 10 days. This failed to influence blood pressure or plasma volume. 3. Antagonist blockade after low salt lowered blood pressure in three patients with the highest plasma renin values. Cardiac output rose in two of these, but it dropped in all others. 4. Decreases in cardiac output occurred with both doses of saralasin and even with suppression of the renin-angiotensin axis. This response is therefore unlikely to be due to removal of myocardial or venous angiotensin effects. 5. The renin-angiotensin system played a part in maintenance of blood pressure only with severe salt restriction and in a small proportion of cases. 6. No heart rate effect was seen with saralasin. 7. Blood pressure and total peripheral resistance responses were dependent on pre-(antagonist/ agonist) setting, but heart rate and cardiac output were not influenced by this factor.

Hemodynamic, hormonal, and renal effects of adrenomedullin in conscious sheep

1997 ◽  
Vol 272 (6) ◽  
pp. R2040-R2047 ◽  
Author(s):  
C. J. Charles ◽  
M. T. Rademaker ◽  
A. M. Richards ◽  
G. J. Cooper ◽  
D. H. Coy ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Right Atrial ◽  
Controlled Study ◽  
Plasma Norepinephrine ◽  
Pressure Lowering ◽  
Conscious Sheep

Adrenomedullin is a recently discovered peptide that has been shown to reduce arterial pressure and induce natriuresis. However, few studies have examined the biological actions of adrenomedullin in conscious animals in an integrative manner. Accordingly, we have examined the hemodynamic, renal, and endocrine actions of adrenomedullin infused intravenously at 10 and 100 ng.kg-1.min-1 (each 90 min) in a vehicle-controlled study in eight normal conscious sheep. Adrenomedullin reduced right atrial pressure (P < 0.05) and diastolic (15 mmHg, P < 0.01) and mean arterial pressure (10 mmHg, P < 0.05) and increased cardiac output (3 l/min, P < 0.001). Total peripheral resistance was reduced 40% (P < 0.001). Urinary sodium was reduced to 35% of control during the 90-min clearance period immediately postinfusion (P < 0.05). Adrenomedullin increased plasma adenosine 3',5'-cyclic monophosphate levels (P < 0.001). Plasma renin activity was elevated during adrenomedullin (P < 0.001) coincident with the peak hypotensive effect, whereas plasma aldosterone was not affected and plasma norepinephrine levels fell (P < 0.05). In conclusion, adrenomedullin had clear blood pressure-lowering effects with increased cardiac output and stimulation of renin but suppressed sympathetic activation in conscious sheep. The physiological implications of these findings require further study.

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