Cardiovascular and renin responses to desmopressin in humans: role of prostacyclin and beta-adrenergic systems

1991 ◽  
Vol 260 (4) ◽  
pp. H1031-H1036 ◽  
Author(s):  
K. Hasunuma ◽  
K. Yamada ◽  
Y. Tamura ◽  
S. Yoshida
Keyword(s):  
Blood Pressure ◽  
Pulse Rate ◽  
Plasma Renin ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Receptor Activation ◽  
Renin Release ◽  
Beta Adrenoceptor ◽  
V2 Receptor

To investigate the involvement of prostacyclin and the sympathetic nervous system in cardiovascular responses to 1-desamino-8-D-arginine vasopressin (DDAVP), a selective V2-receptor agonist, in normal subjects, DDAVP (0.4 micrograms/kg) was infused with or without indomethacin, a cyclooxygenase inhibitor, or propranolol, a beta-adrenoceptor antagonist. A decrease in blood pressure and increases in pulse rate and plasma renin activity (PRA) were observed by DDAVP infusion. Indomethacin did not influence the DDAVP-induced changes in blood pressure and pulse rate but suppressed the increases in PRA and urinary 6-ketoprostaglandin F1 alpha excretion after DDAVP infusion. Even with propranolol administration, DDAVP produced a similar decrease in blood pressure with a reduction of the increased pulse rate. The DDAVP-induced increase in PRA was not affected either. Indomethacin or propranolol alone did not affect the basal levels of the parameters. DDAVP stimulated the in vitro renin release from rabbit renal cortical slices. The stimulation was inhibited by indomethacin or d(CH2)5[D-Ile2,Ile4]AVP, a selective V2-receptor antagonist. These findings suggest that DDAVP primarily elicits vasodilation, probably through the prostacyclin-independent endothelium-derived relaxation and DDAVP also causes an increase in renin release, which would be partly attributed to the increased synthesis of prostacyclin due to vasculoendothelial V2-like receptor activation but not mainly due to an increase in sympathetic nerve activity.

Analysis of beta-adrenoceptors mediating renin release produced by isoproterenol in conscious dogs

1980 ◽  
Vol 238 (5) ◽  
pp. F387-F393
Author(s):  
N. Himori ◽  
A. Izumi ◽  
T. Ishimori
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oral Dose ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Renin Release ◽  
Blocking Drug ◽  
Beta Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Beta 2

Types of beta-adrenoceptors mediating renin release induced by isoproterenol were investigated in conscious dogs. The nonselective beta-adrenoceptor blocking drugs propranolol, D-32, and pindolol significantly inhibited increases in heart rate and plasma renin activity and a fall of blood pressure produced by intravenous infusion of isoproterenol (10 microgram . kg-1 . 20 min-1). d-Propranolol and d-D-32 did not inhibit these three responses to isoproterenol. The selective beta 1-adrenoceptor blocking drug atenolol, at the oral dose of 6 mg/kg, which selectively suppressed isoproterenol-induced tachycardia, significantly inhibited the renin release caused by isoproterenol. By contrast, the renin release induced by isoproterenol was not modified by the selective beta 2-adrenoceptor blocking drug IPS-339 at an oral dose of 3 mg/kg, which fully and selectively antagonized the fall of blood pressure in response to isoproterenol. There was good correlation between suppression of isoproterenol-induced renin release and that of isoproterenol-induced tachycardia after various beta-adrenoceptor blocking drugs. These results lead to the conclusion that in conscious dogs the beta-adrenoceptors mediating release are mainly of the beta 1 type.

Acute Effects of Captopril on Blood Pressure and Circulating Hormone Levels in Salt-Replete and Depleted Normal Subjects and Essential Hypertensive Patients

1981 ◽  
Vol 61 (1) ◽  
pp. 75-83 ◽  
Author(s):  
J. A. Millar ◽  
B. P. McGrath ◽  
P. G. Matthews ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Pulse Rate ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Primary Role ◽  
Ang Ii ◽  
Acute Effects ◽  
Mean Values ◽  
Plasma Renin Concentration

1. The acute effects of a single oral dose of captopril on blood pressure, pulse rate and circulating levels of angiotensin I (ANG I), angiotensin II (ANG II), renin, bradykinin and catecholamines were studied in three groups: eight normal subjects, six salt-depleted normal subjects and 16 patients with essential hypertension. 2. Captopril treatment did not cause any significant fall in supine blood pressure in salt-replete normal subjects or patients with untreated essential hypertension but was associated with a fall in mean blood pressure from 85 ± 2 to 75 ± 2 mmHg in salt-depleted normal subjects and from 131 ± 7 to 117 ± 5 mmHg in patients with essential hypertension treated with diuretics. There was no change in pulse rate in any group. 3. Hormonal responses to captopril were qualitatively similar in the three groups and consisted of significant falls in ANG II with corresponding increases in ANG I and plasma renin concentration. The changes in plasma renin concentration and ANG I were greater in salt-depleted normal subjects (mean values at 90 min were 1140% and 990% of basal levels respectively) than in salt-replete normal subjects (410%, 190%) and were blunted in patients with essential hypertension (140%, 120%). Blood bradykinin, noradrenaline and adrenaline concentrations did not change after captopril in any group. 4. The parallel fall in blood pressure and ANG II levels in salt-depleted normal subjects is consistent with maintenance of blood pressure by increased levels of ANG II in sodium depletion. 5. The failure of captopril to reduce acutely blood pressure in patients with essential hypertension despite suppression of plasma ANG II and without change in circulating bradykinin confirms that the renin-angiotensin system does not play a primary role in essential hypertension.

Effect of reserpine on cardiovascular response to smoking

1962 ◽  
Vol 17 (3) ◽  
pp. 471-474 ◽  
Author(s):  
Thomas C. Westfall ◽  
Daniel T. Watts
Keyword(s):  
Blood Pressure ◽  
Pulse Rate ◽  
Pressure Pulse ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Finger Temperature ◽  
Temperature Changes ◽  
Maximum Change ◽  
Before And After

It has been shown that blood pressure and pulse rate are increased and skin temperature of the extremities is decreased when normal subjects smoke two-thirds of two cigarettes during a period of about 15 min. This standard smoking test has been performed on university students before and after treatment with reserpine (0.25 mg daily) to determine the effect of reserpine on cardiovascular responses to smoking. Blood pressure, pulse rate, finger and toe temperature changes were recorded before and during the smoking test in untreated students and after administration of reserpine for 14 days. The maximum change from control values in ten untreated students and after 14 days of reserpine, respectively, along with P values for differences were as follows: systolic blood pressure (mm Hg) +17, +8, P < .001; diastolic blood pressure (mm Hg) +14, +7, P < .001; pulse rate (beats/ min) +27, +13, P < .001; finger temperature (F) -6.4, -4.0, P < .1; toe temperature (F) -2.7, -4.2. Results show that the characteristic increase in blood pressure and pulse rate and, to a lesser extent, the decrease in finger temperature due to smoking are reduced by pretreatment with reserpine. Submitted on July 10, 1961

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

Effect of linoleic acid infusion on blood pressure in normotensive and hypertensive rats

1989 ◽  
Vol 257 (2) ◽  
pp. H611-H617 ◽  
Author(s):  
S. R. Reddy ◽  
R. Talwalkar ◽  
J. Downs ◽  
T. A. Kotchen
Keyword(s):  
Blood Pressure ◽  
Linoleic Acid ◽  
Sodium Chloride ◽  
Enzymatic Activity ◽  
Plasma Renin ◽  
Sprague Dawley ◽  
Acid Infusion ◽  
High Sodium ◽  
Hypotensive Response

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.

γ-l-Glutamyl-l-Dopa is a Dopamine Pro-Drug, Relatively Specific for the Kidney in Normal Subjects

1985 ◽  
Vol 69 (2) ◽  
pp. 207-214 ◽  
Author(s):  
D. P. Worth ◽  
J. N. Harvey ◽  
J. Brown ◽  
M. R. Lee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Glomerular Filtration Rate ◽  
Plasma Renin Activity ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Urinary Sodium Excretion ◽  
Systemic Effects

1. γ-l-Glutamyl-l-dopa was given by intravenous infusion to eight normal subjects at doses of 12.5 and 100 μg min−1 kg−1. 2. Both doses of the dipeptide resulted in an increase in mean urinary sodium excretion. 3. Mean effective renal plasma flow rose at both doses, but mean glomerular filtration rate increased only at the lower dose. 4. There was a fall in mean plasma renin activity after the infusion of both 12.5 and 100 μg min−1kg−1. 5. Mean urine free dopamine excretion increased by 280- and 2500-fold at infusion rates of 12.5 and 100 μg min−1 kg−1 respectively. 6. Mean plasma free dopamine rose at both doses but the increase at 12.5 μg min−1 kg−1 was not to a level previously associated with systemic effects of the catecholamine. 7. On administration of the dipeptide at 12.5 μg min−1 kg−1 there were no changes in blood pressure or heart rate, but at the higher dose there was a fall in diastolic blood pressure. 8. At a dose of 12.5 μg min−1 kg−1 in man, there is kidney specific conversion of gludopa to dopamine.

Blocking properties of terguride at the 5-HT2 receptor subtypes mediating cardiovascular responses in the rat

2020 ◽  
Vol 98 (8) ◽  
pp. 511-521
Author(s):  
Oscar Alcántara-Vázquez ◽  
Ma. Trinidad Villamil-Hernández ◽  
Araceli Sánchez-López ◽  
Heinz H. Pertz ◽  
Carlos M. Villalón ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Diastolic Blood Pressure ◽  
Receptor Agonist ◽  
Cardiovascular Responses ◽  
Receptor Subtypes ◽  
Pithed Rats ◽  
Anaesthetized Rats ◽  
Dose Dependent

In vitro studies have suggested that terguride blocks the contractile and relaxant responses produced by 5-hydroxytryptamine (5-HT) via 5-HT2A/2B receptors. This study has now investigated terguride’s blocking properties on central/peripheral 5-HT2 receptors in anaesthetized or pithed rats. Male Wistar anaesthetized/pithed rats were cannulated for recording blood pressure and heart rate and for i.v. administration of several compounds. In both groups of rats, i.v. bolus injections of 5-HT or (±)-DOI (a 5-HT2 receptor agonist; 1–1000 μg/kg) produced dose-dependent increases in diastolic blood pressure and heart rate. These responses were dose-dependently antagonized by terguride (10–3000 μg/kg). In anaesthetized rats, i.v. bolus injections of BW723C86 (a 5-HT2B receptor agonist; 1–1000 μg/kg) produced dose-dependent increases in diastolic blood pressure and not dose-dependent increases in heart rate, while in pithed rats, these responses were attenuated. The vasopressor responses elicited by BW723C86 in anaesthetized rats were dose-dependently blocked by terguride (10–300 μg/kg), whereas its the tachycardic responses were dose-independently blocked. These results, taken together, suggest that terguride behaved as an antagonist at the 5-HT2 receptors located in the central nervous system and (or) the systemic vasculature. This is the first evidence demonstrating that terguride can block central/peripheral 5-HT2 receptors mediating cardiovascular responses in anaesthetized or pithed rats.

Glyburide attenuates calmodulin antagonist-stimulated renin release from isolated mouse juxtaglomerular cells

1995 ◽  
Vol 269 (2) ◽  
pp. F242-F247 ◽  
Author(s):  
D. A. Linseman ◽  
J. A. Lawson ◽  
D. A. Jones ◽  
J. H. Ludens
Keyword(s):  
Calcium Release ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
K Channel ◽  
Inhibitory Effects ◽  
Calmodulin Antagonist ◽  
Voltage Gated Calcium Channels

Previous reports have shown that K+ channel openers elevate plasma renin activity in vivo and stimulate renin release (RR) from juxtaglomerular (JG) cells in vitro. Therefore, we examined whether the K+ channel blocker, glyburide, inhibits basal RR or RR stimulated by elevating cAMP or by inhibiting Ca2+/calmodulin activity in cultures of isolated mouse JG cells. Glyburide treatment (10-300 microM) had no effect on basal RR, which measured approximately 10% or 30% of the total cellular renin activity after 4 or 24 h, respectively. RR stimulated by elevating cAMP with isoproterenol, forskolin, or 3-isobutyl-1-methylxanthine was also unaffected by glyburide. In contrast, glyburide significantly attenuated RR stimulated by the calmodulin antagonists, calmidazolium, trifluoperazine, and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7). Calmidazolium-stimulated RR returned to basal levels with 100 microM glyburide cotreatment. Blockade of voltage-gated calcium channels with verapamil or inhibition of calcium release from intracellular stores with 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8) had no effect on the ability of glyburide to attenuate calmidazolium-stimulated RR. However, lowering of the extracellular calcium concentration by the addition of EGTA abolished the inhibitory effects of glyburide. We conclude that modulation of K+ channels may influence RR by affecting Ca2+/calmodulin-regulated secretion, but not cAMP-mediated secretion, from JG cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Behavioural and cardiovascular responses of rats to euthanasia using carbon dioxide gas

1997 ◽  
Vol 31 (4) ◽  
pp. 337-346 ◽  
Author(s):  
William Smith ◽  
Stephen B. Harrap
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Pulse Rate ◽  
Gas Flow ◽  
Cardiovascular Responses ◽  
Carbon Dioxide Gas ◽  
Apparent Death ◽  
Signs Of Death ◽  
Behavioural Evidence

Our results showed more rapid falls in pulse rate and blood pressure in rats euthanized in a chamber precharged with carbon dioxide (CO2), when compared with rats euthanized more slowly, but death still took over 5 min in the former group. There was no behavioural evidence of pain or distress in either group during euthanasia. Initial ataxia and dyspnoea was punctuated by a lag before death, thus separating euthanasia into three clearly defined phases. All visual signs of death preceded complete vascular collapse by about 1 min in both groups, so we recommend that gas flow be maintained for at least 1 min after apparent death.

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