Unchanged sensitivity to noradrenaline in isolated tissues from cold-acclimated rats

1970 ◽  
Vol 48 (9) ◽  
pp. 657-660 ◽  
Author(s):  
Jean Himms-Hagen ◽  
I. M. Mazurkiewicz-Kwilecki
Keyword(s):  
Left Atrium ◽  
Vas Deferens ◽  
Contractile Response ◽  
Cardiovascular Responses ◽  
Maximum Response ◽  
Inotropic Response ◽  
Chronotropic Response ◽  
Isolated Atria ◽  
Isolated Tissues

Acclimation of rats to cold did not alter either the sensitivity to noradrenaline or the size of the maximum response to noradrenaline of three isolated tissue preparations (chronotropic response of isolated atria; inotropic response of left atrium; contractile response of vas deferens). It is concluded that a change in the response of the heart to exogenous noradrenaline is an unlikely explanation for the modified cardiovascular responses to noradrenaline known to occur in intact cold-acclimated rats.

Dietary manipulation of cardiac and aortic smooth muscle reactivity to isoproterenol

1984 ◽  
Vol 246 (3) ◽  
pp. H369-H373 ◽  
Author(s):  
J. T. Herlihy
Keyword(s):  
Body Weight ◽  
The Body ◽  
Heart Weight ◽  
Inotropic Response ◽  
Chronotropic Response ◽  
Fischer 344 ◽  
Isolated Atria ◽  
Group A ◽  
The Right ◽  
Right Atria

The responsiveness to isoproterenol of isolated atria and aortic strips was examined in two groups of male Fischer 344 rats. Group A (control) was composed of 5-mo-old rats fed ad libitum; group R (experimental) was composed of rats whose food intake had been restricted for 2 mo to 60% of that consumed by group A. Aortic strips obtained from group R and preconstricted with 30 mM K+ relaxed by 18% when challenged by a maximal concentration of isoproterenol (1 microM). This relaxation was significantly less than the 28% relaxation observed with strips from group A. No effect on the inotropic response of the left atria or on the chronotropic response of the right atria to maximal concentrations of isoproterenol was observed. A slight but statistically significant increase in sensitivity to isoproterenol was observed in the inotropic response of the left atria. The 50% effective concentration (EC50) for the isoproterenol-stimulated increase in force development observed with group R was 0.87 +/- 0.16 X 10(-8) M, which was significantly less than the value of 1.56 +/- 0.28 X 10(-8) M obtained with atria from group A. Food restriction exerted no significant effect on the EC50 for the chronotropic response of right atria to isoproterenol. Both the body weight and the heart weight of group A were greater than those of group R. However, the ratio of heart weight to body weight was significantly greater in group R than in group A.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of histamine on rat isolated atria

1980 ◽  
Vol 58 (9) ◽  
pp. 1114-1116 ◽  
Author(s):  
I. Laher ◽  
J. H. McNeill
Keyword(s):  
Muscarinic Receptors ◽  
Right Atrium ◽  
Inotropic Response ◽  
Chronotropic Response ◽  
Adrenoceptor Antagonist ◽  
Endogenous Noradrenaline ◽  
Isolated Atria ◽  
High Doses ◽  
Indirect Stimulation ◽  
Stimulation Of

The effects of histamine were studied in atria obtained from untreated and reserpine-pretreated rats. At high doses, histamine caused a positive chronotropic response that was not antagonized by either promethazine or cimetidine. In the presence of propranolol or in atria from reserpine-pretreated rats histamine caused an atropine-sensitive negative chronotropic response. Large doses of histamine also caused a positive inotropic response in left atria that were antagonized by the β adrenoceptor antagonist propranolol. Reserpine pretreatment abolished the inotropic response of histamine in the rat heart. The results indicate that in large doses histamine causes an indirect stimulation of β adrenoceptors (right and left atrium) by releasing endogenous noradrenaline and of muscarinic receptors (right atrium) by releasing acetylcholine.

The effect of pH on rabbit atrial response to histamine

1976 ◽  
Vol 54 (2) ◽  
pp. 118-127 ◽  
Author(s):  
M. J. Hughes ◽  
I. A. Coret
Keyword(s):  
Histamine Receptor ◽  
Maximum Response ◽  
Force Of Contraction ◽  
Histamine Concentration ◽  
Adenyl Cyclase Activity ◽  
Chronotropic Response ◽  
Spontaneous Rate ◽  
Histamine Response ◽  
Ph Range ◽  
Rabbit Atria

The chronotropic response of isolated rabbit atria in normal Tyrode's medium increases monotonically with increasing doses of histamine (9 × 10−7–9 × 10−4 M). Plots of the inverse of response against the inverse of concentration were linear; and from these plots were derived values for the theoretical maximum response at 'infinite' dose and for the histamine concentration required to evoke a half maximum response. Alteration of pH by changing [HCO3−] at constant pCO2, [Na+] and osmolality did not appreciably affect the response to histamine in the range pH 7.0–7.6. However, at pH below 7.0 the magnitude of histamine response was reduced at all concentrations of histamine tested. In the pH range 7.0–7.6, additions of NaHCO3 at constant pCO2 increased the spontaneous rate of rabbit atria (in the absence of histamine); however, there was little effect of changing pH (in this range) by altering [HCO3−] at constant pCO2 when [Na+] and osmolality were kept constant. Immersion in solutions at pH's less than 7.0 led to decline in spontaneous rate and force of contraction. It is probable that depression of adenyl cyclase activity rather than a specific change in ionization of histamine receptor is responsible for a decreased response to histamine at pH 6.9.

Effect of nicotine on cardiac muscle contractions and radiocalcium movement

1963 ◽  
Vol 205 (5) ◽  
pp. 890-896 ◽  
Author(s):  
Winifred G. Nayler
Keyword(s):  
Cardiac Muscle ◽  
Contractile Response ◽  
Muscle Contractions ◽  
Ventricular Muscle ◽  
Inotropic Response ◽  
Uptake And Release

Nicotine, 0.01–0.1 mm, evoked a positive inotropic response and abolished the "staircase" and poststimulation potentiation in toad ventricular muscle; 0.2 mm nicotine caused the development of contracture, whether or not extracellular Ca++ was present; and 1.0 mm nicotine enhanced the uptake and release of Ca45 from the muscle. It seems probable that the effect of nicotine on the contractile response of cardiac muscle can be related to the mobilization of Ca++.

Renal microvascular effects of endothelin

1990 ◽  
Vol 259 (2) ◽  
pp. F217-F221 ◽  
Author(s):  
R. M. Edwards ◽  
W. Trizna ◽  
E. H. Ohlstein
Keyword(s):  
Response Curve ◽  
Contractile Response ◽  
Maximum Response ◽  
Lumen Diameter ◽  
Rabbit Kidney ◽  
Significant Shift ◽  
Efferent Arteriole ◽  
Endothelin 1 ◽  
Afferent Arterioles ◽  
Concentration Response Curve

The effects of endothelin 1, 2, and 3 (ET-1, -2, -3) on lumen diameter of individual afferent and efferent arterioles dissected from rabbit kidney were examined. ET-1 produced concentration-dependent and long-lasting decreases in lumen diameter in both arterioles. The 50% maximum response (EC50) values were 1.4 +/- 0.41 and 0.9 +/- 0.65 nM for afferent and efferent arterioles, respectively. In afferent arterioles, ET-2 produced decreases in lumen diameter (EC50 = 3.3 +/- 1.75 nM) that were indistinguishable from ET-1. However, ET-3 was considerably less potent (EC50 = 21.9 +/- 6.0 nM, P less than 0.05) than ET-1 or ET-2. Similar results were obtained in the efferent arteriole in which the EC50 for ET-2 (0.25 +/- 0.1 nM) was similar to ET-1, but ET-3 was significantly less potent (EC50 = 2.6 +/- 0.4 nM, P less than 0.05). Nicardipine (0.01-1 microM) produced concentration-dependent shifts in the ET-1 concentration-response curve in afferent arterioles. Verapamil (1 microM) also caused a significant shift in the ET-1 response curve. The contractile response to ET-1 was significantly more sensitive to nicardipine than was the response to norepinephrine. In contrast, the response of efferent arterioles to ET-1 and norepinephrine was unaffected by nicardipine or verapamil. The results demonstrate that ETs are potent vasoconstrictors of both the pre- and postglomerular microvasculature and may play a role in the regulation of renal hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of vagal feedback from the lung in hypoxic-induced tachycardia in humans

1995 ◽  
Vol 78 (4) ◽  
pp. 1522-1530 ◽  
Author(s):  
P. M. Simon ◽  
B. H. Taha ◽  
J. A. Dempsey ◽  
J. B. Skatrud ◽  
C. Iber
Keyword(s):  
Lung Transplant ◽  
Human Subjects ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Chronotropic Response ◽  
Transplant Patients ◽  
Marked Variability ◽  
Arterial O2 Saturation ◽  
Mild Hypoxia

We assessed the cardiovascular responses to systemic normocapnic hypoxia in five normal subjects, five double lung transplant patients with lung denervation and intact hearts, and five patients with denervated hearts. Progressive normocapnic hypoxia was induced over 10–15 min and maintained for 2–3 min each at 90, 87, 84, and 80% arterial O2 saturation (SaO2). Normal subjects showed the most pronounced mean increase in heart rate (dHR/dSaO2 = 0.86 +/- 0.13 beat/min per 1% SaO2). Three lung-denervated subjects had normal tachycardiac responses (1.6, 0.9, and 0.69 beats/min per 1%), whereas the other two had distinctly lower responses (0.34 and 0.39 beat/min per 1%). Most of the lung-denervated subjects also showed a significant tachycardia with even mild hypoxia; none showed a bradycardiac response to any level of hypoxia. In the heart-denervated group, hypoxic tachycardia was significantly lower than normal (0.29 +/- 0.13 beat/min per 1%). We conclude that vagal feedback from the lungs is not required for the normal chronotropic response to hypoxia in humans; however, this mechanism may contribute significantly to the marked variability in hypoxic-induced tachycardia found among human subjects. These data in humans contrast with the progressive bradycardiac response to hypoxia reported in vagally denervated (or nonhyperpneic) dogs and cats.

Evidence for ATP and noradrenaline as cotransmitters in sympathetic nerves

1985 ◽  
Vol 68 (s10) ◽  
pp. 89s-92s ◽  
Author(s):  
G. Burnstock ◽  
P. Sneddon
Keyword(s):  
Guinea Pig ◽  
Experimental Evidence ◽  
Ad Hoc ◽  
Vas Deferens ◽  
Contractile Response ◽  
Alternative Hypothesis ◽  
Smooth Muscles ◽  
Sympathetic Nerves ◽  
Apparent Contradiction ◽  
Nerve Muscle

Sympathetically innervated smooth muscles, including those in some arteries, arterioles, cat nictitating membrane and vas deferens, have α1-adrenoceptors which respond to exogenously applied noradrenaline (NA) by producing contractions which can be abolished by α1-adrenoceptor antagonists such as prazosin. Stimulation of the sympathetic nerves innervating these muscles causes release of NA and a contractile response. However, this contraction is (at least partly) resistant to specific α1-adrenoceptor antagonists. This apparent contradiction could be explained by a variety of ad hoc explanations (such as high transmitter concentrations within the nerve-muscle junction, or prejunctional enhancement of transmitter release by the antagonist due to prejunctional α2-adrenoceptor blockade etc.) but recently two hypotheses have been advanced which may have more fundamental implications for sympathetic neurotransmission. First, Hirst and Neild and their colleagues suggested that the electrical and mechanical responses of some smooth muscles were resistant to α-adrenoceptor antagonists because neuronally released NA was acting not only on α-adrenoceptors but also on a new class of adrenoceptors which they designated γ-receptors, located near the nerve-muscle junction. The crucial experiments in support of this hypothesis were originally performed on the arterioles of the guinea-pig submucosa [1], but the idea has been extended to include many other sympathetically innervated smooth muscles [2], including guinea-pig vas deferens, which was also the smooth muscle preparation in which the experimental evidence for an alternative hypothesis was obtained by Fedan et al. [3]. They proposed that the α-blocker-resistant portion of the contractile response to sympathetic nerve stimulation was mediated by ATP, acting as a cotransmitter with NA. Full details of the early development of the concept of cotransmission in sympathetic nerves have been reviewed previously [4, 6, 7]. The experimental evidence relating to the co-transmission hypothesis is outlined below, drawing mainly on results obtained in guinea-pig vas deferens, where most of the more recent experiments have been performed.

Sign in / Sign up

Export Citation Format

Share Document