Adenosine and Cardiovascular Function

Mullane, Kevin; Williams, Michael

doi:10.1007/978-1-4612-4504-9_8

Cited by 28 publications

(17 citation statements)

References 155 publications

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“…In addition to those tissues found to express the Al receptor gene by Northern blot analysis (brain, spinal cord, epididymis plus vas deferens, testis white adipose tissue, stomach, spleen, pituitary and adrenal, Reppert et al, 1991), we detected Al receptor mRNA in the heart, aorta, kidney, liver, eye and bladder. Functional effects of the Al receptor in the periphery have been observed in the heart (Mullane & Williams, 1990), the spleen (Fozard & Milavec-Krizman, 1993), the liver (Ohigashi et al, 1993), the eye (Blazynski, 1990), the aorta (Conti et al, 1993), the stomach (Christofi et al, 1992), the colon (Jarvis et al, 1994) and the bladder (Foster & Ferguson, personal communication). Al receptor mRNA has also been previously found in the testis (Rivkees, 1994), spleen and liver (Stehle et al, 1992).…”

Section: Discussionmentioning

confidence: 99%

Tissue distribution of adenosine receptor mRNAs in the rat

Dixon

Gubitz

Sirinathsinghji

et al. 1996

British J Pharmacology

518

345

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1 A degree of ambiguity and uncertainty exists concerning the distribution of mRNAs encoding the four cloned adenosine receptors. In order to consolidate and extend current understanding in this area, the expression of the adenosine receptors has been examined in the rat by use of in situ hybridisation and the reverse transcription-polymerase chain reaction (RT-PCR). 2 In accordance with earlier studies, in situ hybridisation revealed that the adenosine A1 receptor was widely expressed in the brain, whereas A2A receptor mRNA was restricted to the striatum, nucleus accumbens and olfactory tubercle. In addition, A1 receptor mRNA was detected in large striatal cholinergic interneurones, 26% of these neurones were also found to express the A2A receptor gene. Central levels of mRNAs encoding adenosine A2B and A3 receptors were, however, below the detection limits of in situ hybridisation. 3 The more sensitive technique of RT-PCR was then employed to investigate the distribution of adenosine receptor mRNAs in the central nervous system (CNS) and a wide range of peripheral tissues.As a result, many novel sites of adenosine receptor gene expression were identified. Al receptor expression has now been found in the heart, aorta, liver, kidney, eye and bladder. These observations are largely consistent with previous functional data. A2A receptor mRNA was detected in all brain regions tested, demonstrating that expression of this receptor is not restricted to the basal ganglia. In the periphery A2A receptor mRNA was also found to be more widely distributed than generally recognised. The ubiquitous distribution of the A2B receptor is shown for the first time, A2B mRNA was detected at various levels in all rat tissues studied. Expression of the gene encoding the adenosine A3 receptor was also found to be widespread in the rat, message detected throughout the CNS and in many peripheral tissues. This pattern of expression is similar to that observed in man and sheep, which had previously been perceived to possess distinct patterns of A3 receptor gene expression in comparison to the rat. 4 In summary, this work has comprehensively studied the expression of all the cloned adenosine receptors in the rat, and in so doing, resolves some of the uncertainty over where these receptors might act to control physiological processes mediated by adenosine.

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Section: Discussionmentioning

confidence: 99%

Tissue distribution of adenosine receptor mRNAs in the rat

Dixon

Gubitz

Sirinathsinghji

et al. 1996

British J Pharmacology

518

345

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“…We also found that the embryos were smaller after maternal CPA injections, indicating that there was intrauterine growth retardation. Because adenosine can influence maternal vascular function and possibly affect placental blood flow (Mullance and Williams, 1990;, it is possible that the effects observed in utero reflected these factors. Thus, to overcome this potential limitation we studied isolated intact embryos.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of cell proliferation in the embryonic myocardium by A1 adenosine receptor activation

Zhao

Rivkees

2001

Developmental Dynamics

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A1 adenosine receptors (A1ARs) are expressed in the embryonic heart and influence cardiac function at early developmental stages. To test if A1ARs also affect cardiac structural development, we examined the effects of A1AR activation on heart formation. When pregnant mice were treated with the A1AR agonist, N 6 -cyclopentyladenosine (CPA), fetuses showed marked reduction of ventricular size and manifested features of heart failure. Suggesting that these findings represent direct effects on embryos, CPA treatment of cultured whole murine embryos resulted in cardiac hypoplasia. When rates of cell division and cell death in the heart were examined, we found decreases in cardiac cell proliferation following A1AR activation. In contrast, no changes in numbers or distribution of apoptotic cells were seen. Collectively, these data show that A1AR activation inhibits cardiac cell proliferation and can lead to cardiac hypoplasia. These data identify adenosine as a potential regulator of cardiac cell division during early development.

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“…Increased blood flow, inhibition of granulocyte adherence, and less tissue injury were observed. One mechanism proposed for the cardiac protective effects of AICA riboside is an increased production of adenosine rather than inosine from ATP catabolism although the precise mechanism for this effect has yet to be determined [61].…”

Section: Adenosine Potentiatorsmentioning

confidence: 99%

Novel therapeutics acting via purine receptors

Jacobson

Trivedi²,

Churchill

et al. 1991

Biochemical Pharmacology

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A recent conference entitled Purines in Cell Signalling: Targets for New Drugs, held in Rockville, Maryland, in September, 1989, was one indication of the increasing interest in developing agonists and antagonists of P 1 -(adenosine) and P 2 -(ATP) purinoceptors [1] as potential therapeutic agents. Extracellular adenosine, acting at its membrane bound A 1 and A 2 receptors, is a ubiquitous modulator of cellular activity. The purine can arise from several sources including ATP hydrolysis by ectokinase activity in the region of the nerve terminal [2] and from S-adenosylhomocysteine [3] and ATP within the cell. Together with its more stable analogs, adenosine is a potent inhibitor of neurotransmitter release in both the central and peripheral nervous systems, and in cardiac, adipose and other tissues. Adenosine can also affect blood pressure and heart rate as well as modulate the function of the immune, inflammatory, gastrointestinal, renal and pulmonary systems, either via its effects on transmitter release or directly via receptor mechanisms altering intracellular transduction processes.

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Adenosine and Cardiovascular Function

Cited by 28 publications

References 155 publications

Tissue distribution of adenosine receptor mRNAs in the rat

Tissue distribution of adenosine receptor mRNAs in the rat

Inhibition of cell proliferation in the embryonic myocardium by A1 adenosine receptor activation

Novel therapeutics acting via purine receptors

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