Modulation of in vitro erythropoiesis. The influence of beta-adrenergic agonists on erythroid colony formation.

SUMMARYWe previously reported that blood forms of Trypanosoma cruzi express alpha- and beta-adrenergic receptors and that binding of specific agonists to these receptors modifies the infective capacity of the parasite in vitro. The present study has revealed that the inhibitory effect of the beta-adrenergic agonist L-isoproterenol and the stimulatory effect of the alpha-adrenergic agonist L-phenylephrine are not produced when the parasite is subjected to prolonged exposure to otherwise effective doses of these agonists or when supraoptimal doses of these agonists are used. We refer to these phenomena as ‘desensitization’ because of their analogy with vertebrate cells becoming desensitized by prolonged exposure to, or relatively high concentrations of, adrenergic agonists. At a constant agonist concentration, T. cruzi desensitization was time-dependent and, when the time of parasite treatment with the agonists was not changed, the higher concentrations of the agonist tested were the most effective in producing desensitization. The reduced infectivity resulting from treatment with optimal doses of L-isoproterenol was accompanied by elevated levels of cyclic adenosine mono- phosphate (cAMP) which were not detectable when L-isoproterenol concentrations producing desensitization were used. This finding implicated cAMP as a likely second signal in the inhibitory mechanisms of this agonist. No significant change in cAMP was detectable in parasites treated with L-phenylephrine, leaving open the question about how optimal doses of this alpha-adrenergic agonist enhance T. cruzi infectivity. Parasite responsiveness to alpha- and beta-adrenergic agonists as well as the desensitization effects define a system which regulates infectivity and could be modified at the host tissue level by naturally occurring agonists.

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Pharmacological Agents and Erythroid Colony Formation: Effects of Beta-Adrenergic Agonists and Steroids

In Vitro Aspects of Erythropoiesis ◽

10.1007/978-1-4612-6301-2_18 ◽

1978 ◽

pp. 103-117 ◽

Cited By ~ 2

Author(s):

James W. Fisher ◽

Yasuchico Ohno ◽

Bruno Modder ◽

Franciszek Przala ◽

Gregory D. Fink ◽

...

Keyword(s):

Colony Formation ◽

Adrenergic Agonists ◽

Beta Adrenergic ◽

Pharmacological Agents ◽

Beta Adrenergic Agonists

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Decreased insulin binding to porcine adipocytes in vitro by beta-adrenergic agonists.

Journal of Animal Science ◽

10.2527/1990.6861603x ◽

1990 ◽

Vol 68 (6) ◽

pp. 1603 ◽

Cited By ~ 13

Author(s):

C Y Liu ◽

S E Mills

Keyword(s):

Insulin Binding ◽

Adrenergic Agonists ◽

Beta Adrenergic ◽

Beta Adrenergic Agonists ◽

Porcine Adipocytes

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Prolonged administration in vivo of alpha and beta adrenergic agonists decreases insulin binding to rat myocardial membranes in vitro by different mechanisms

Life Sciences ◽

10.1016/0024-3205(91)90340-h ◽

1991 ◽

Vol 48 (23) ◽

pp. 2249-2258 ◽

Cited By ~ 3

Author(s):

G. Desoye ◽

U. Ertl-Stockinger ◽

S. Porta

Keyword(s):

Insulin Binding ◽

Adrenergic Agonists ◽

Prolonged Administration ◽

Beta Adrenergic ◽

Beta Adrenergic Agonists ◽

Myocardial Membranes

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The rate of substrate cycling between fructose 6-phosphate and fructose 1,6-bisphosphate in skeletal muscle

Biochemical Journal ◽

10.1042/bj2210153 ◽

1984 ◽

Vol 221 (1) ◽

pp. 153-161 ◽

Cited By ~ 37

Author(s):

R A J Challiss ◽

J R S Arch ◽

E A Newsholme

Keyword(s):

Exchange Chromatography ◽

Adrenergic Agonists ◽

Beta Adrenergic ◽

Cycling Rate ◽

Physiological Importance ◽

Beta Adrenergic Agonists ◽

Fructose 1,6 Bisphosphatase ◽

Adrenergic Antagonists ◽

Fructose 1,6 Bisphosphate

Substrate cycling of fructose 6-phosphate through reactions catalysed by 6-phosphofructokinase and fructose-1,6-bisphosphatase was measured in skeletal muscles of the rat in vitro. The rate of this cycle was calculated from the steady-state values of the 3H/14C ratio in hexose monophosphates and fructose 1,6-bisphosphate after the metabolism of either [5-3H,6-14C]glucose or [3-3H,2-14C] glucose. Two techniques for the separation of hexose phosphates were studied; t.l.c. chromatography on poly(ethyleneimine)-cellulose sheets or ion-exchange chromatography coupled with enzymic conversion. These two methods gave almost identical results, suggesting that either technique could be used for determination of rates of fructose 6-phosphate/fructose 1,6-bisphosphate cycling. It was found that more than 50% of the 3H was retained in the fructose 1,6-bisphosphate; it is therefore probable that previous measurement of cycling rates, which have assumed complete loss of 3H, have underestimated the rate of this cycle. The effects of insulin, adrenaline and adrenergic agonists and antagonists on rates of fructose 6-phosphate/fructose 1,6-bisphosphate cycling were investigated. In the presence of insulin, adrenaline (1 microM) increased the cycling rate by about 10-fold in epitrochlearis muscle in vitro; the maximum rate under these conditions was about 2.5 mumol/h per g of tissue. The concentration of adrenaline that increased the cycling rate by 50% was about 50 nM. This effect of adrenaline appears to be mediated by the beta-adrenergic receptor, since the rate was increased by beta-adrenergic agonists and blocked by beta-adrenergic antagonists. From the knowledge of the precise rate of this cycle, the possible physiological importance of cycling is discussed.

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Sympathetic nervous system and renin release from submaxillary glands in vitro

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.231.2.551 ◽

1976 ◽

Vol 231 (2) ◽

pp. 551-554 ◽

Cited By ~ 5

Author(s):

AM Michelakis ◽

JW Menzie ◽

H Yoshida

Keyword(s):

Direct Action ◽

Submaxillary Gland ◽

Renin Release ◽

Adrenergic Agonists ◽

Beta Adrenergic ◽

Submaxillary Glands ◽

Beta Adrenergic Agonists ◽

Camp Levels

We previously reported that alpha- but not beta-adrenergic agonists stimulate renin release from mouse submaxillary glands in vivo. The present studies were undertaken to determine if these in vivo effects were due to a direct action on the submaxillary glands and to find out if cyclic AMP (cAMP) might be involved in submaxillary renin release. Pooled mouse submaxillary gland slices were incubated in Krebs-Ringer bicarbonate medium following a preincubation period, and renin release was measured by a radioimmunoassay for the direct measurement of submaxillary gland renin. Tissue cAMP levels were also measured. Addition of the alpha-adrenergic agonists, phenylephrine or norepinephrine, significantly increased renin release (P less than 0.01 vs. control) while decreasing tissue cAMP levels (P less than 0.01 vs. control). In contrast, addition of the beta-adrenergic agonist isoproterenol markedly increased cAMP levels (P less than 0.01 vs. control) and decreased renin release (P less than 0.05 vs. control). Pretreatment of the slices with the alpha-blocker phenoxy genzamine inhibited the effect of phenylephrine. These results indicate that alpha-adrenergic agonists cause renin release from submaxillary glands which is accompanied by a fall in tissue cAMP levels. This is in contrast to renin release from the kidney which is stimulated by beta-adrenergic agonists.

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Exercise training and responsiveness of isolated coronary arteries

Journal of Applied Physiology ◽

10.1152/jappl.1991.71.6.2346 ◽

1991 ◽

Vol 71 (6) ◽

pp. 2346-2351 ◽

Cited By ~ 36

Author(s):

P. J. Rogers ◽

T. D. Miller ◽

B. A. Bauer ◽

J. M. Brum ◽

A. A. Bove ◽

...

Keyword(s):

Exercise Training ◽

Coronary Arteries ◽

Vasoactive Intestinal Polypeptide ◽

Adrenergic Agonists ◽

Response Curves ◽

Beta Adrenergic ◽

Beta Adrenergic Agonists ◽

The Right ◽

Intestinal Polypeptide

Exercise is associated with release of catecholamines and vasoactive intestinal polypeptides. Recurrent exposure to catecholamines modifies the sensitivity of adrenoceptors. To test the hypothesis that exercise training may affect the sensitivity of the epicardial coronary arteries, we performed studies on isolated coronary arteries from male dogs capable of running on a treadmill. The animals were separated randomly into two groups: sedentary and exercise training. After 11 wk, rings of left circumflex and left anterior descending coronary arteries were studied in vitro. Contractions to alpha 1-adrenergic agonists (norepinephrine and phenylephrine) were not affected by exercise training. During contractions with prostaglandin F2 alpha, endothelium-dependent relaxations to alpha 2-adrenergic agonists (norepinephrine and UK 14304) were not reduced significantly by exercise training. The concentration-relaxation curves to beta-adrenergic agonists (norepinephrine, isoproterenol, and epinephrine) were shifted to the right after training. The concentration-response curves to vasoactive intestinal polypeptide, but not that to substance P, were shifted to the right in rings with endothelium from exercise-trained animals. These findings demonstrate a decrease in responsiveness of canine vascular smooth muscle to beta-adrenergic agonists and to vasoactive intestinal polypeptide after exercise training.

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