The mechanism of functional vasodilatation in rabbit epigastric adipose tissue

Lewis, George; Matthews, J. M.

doi:10.1113/jphysiol.1970.sp009045

Cited by 31 publications

(11 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This proposal is consistent with our observation that PGI 2 is produced in larger quantity than PGE 2 during NE-induced lipolysis, with the fact that PGI 2 is a more potent vasodilator than PGE 2 , and with the observation that no vasodilator substance could be detected in the venous effluent of the activated adipose tissue, but only from extracts of adipose tissue. 21 The last observation is consistent with the known instability of PGI 2 .…”

Section: Discussionsupporting

confidence: 89%

See 1 more Smart Citation

Prostacyclin Production by Isolated Adipocytes

Axelrod

Levine

1981

Diabetes

View full text Add to dashboard Cite

Isolated rat adipocytes produce prostacyclin (PGI2) in relatively large quantities during norepinephrine (NE)-induced lipolysis. The endogenous NE-induced production rate of PGI2, calculated from the NE-induced production rate of PGI2 observed in our studies (2.2 ng/10(6) cells/2 h) and from the number of fat cells in the normal organism, is 1.46 ng/kg/min for rats, 4.46 ng/kg/min for men, and 11.86 ng/kg/min for women. These rates are comparable to the exogenous PGI2 infusion rate that alters platelet aggregation and blood pressure in rats and humans. Exogenous PGI2 failed to modify the rate of NE-induced lipolysis. Inhibition of endogenous PGI2 production by indomethacin had no effect on the rate of NE-induced lipolysis when either a maximal or submaximal lipolytic concentration of NE was used. PGI2 [rather than prostaglandin (PG) E2] may be the substance that accounts for the functional vasodilatation that accompanies hormone-induced lipolysis. PGI2 is produced in large quantities than PGE2 during NE-induced lipolysis and is a more potent vasodilator than PGE2. Its instability can account for the inability of previous investigators to detect a vasodilator substance in the venous effluent of adipose tissue. The production of PGI2 by adipocytes may be an important modulator of the regulation of vascular tone and platelet aggregation by catecholamines in the vascular bed of adipose tissue and perhaps other tissues. PGI2 produced by adipocytes, by virtue of its ability to cause vasodilatation and inhibit platelet aggregation, may contribute to the maintenance of luminal patency in the vascular bed of adipose tissue and possibly other tissue as well.

show abstract

Section: Discussionsupporting

confidence: 89%

“…21 " 23 When lipolytic substances are infused into the arterial supply of adipose tissue, they also cause an increase in the blood flow to the adipose tissue. 21 This functional dilatation is abolished by indomethacin and aspirin. 23 Although it has been proposed that the vasodilator substance is PGE 2 , 22 ' 23 we suggest that it is PGI 2 .…”

Section: Discussionmentioning

confidence: 98%

Prostacyclin Production by Isolated Adipocytes

Axelrod

Levine

1981

Diabetes

View full text Add to dashboard Cite

show abstract

“…In an earlier paper we showed that activation of rabbit adipose tissue by close arterial injection of lipolytic hormones resembles that in endocrine glands in being prolonged and accompanied by a prolonged increase in blood flow (Lewis & Matthews, 1968). More recently we were able to show that the functional vasodilatation in adipose tissue is accompanied by the release or formation of a vasodilator substance (Lewis & Matthews, 1970). In the present experiments we have examined the nature of the substance.…”

Section: Introductionmentioning

confidence: 96%

“…Lipolytic agents were infused close-arterially to the epigastric adipose tissue as described earlier (Lewis & Matthews, 1970).…”

Section: Methodsmentioning

confidence: 99%

The relationship between functional vasodilatation in adipose tissue and prostaglandin

Bowery¹,

Lewis²,

Matthews³

1970

British J Pharmacology

Self Cite

View full text Add to dashboard Cite

Summary1. Earlier it had been found that during fat mobilization there was an increased blood flow in the adipose tissue and the tissue contained a vasodilator substance. 2. Extract of an activated fat pad contained 3 to 25 times as much activity as the contralateral resting fat pad. 3. The following findings suggest that the vasodilator substance is prostaglandin E2: (a) It caused contractions of the guinea-pig ileum which were not reduced by mepyramine, but were reduced by atropine.(b) It caused a prolonged vasodilator response when injected closearterially to the epigastric fat pad. (c) It was eluted from a silicic acid column by a solvent system which is known to elute prostaglandins of the E series but not those of the F series.(d) Its indices of discrimination were similar to those of prostaglandin E's when assayed on three different pharmacological preparations.(e) On thin-layer chromatography it behaved more like prostaglandin E2 than E1.4. Neither prostaglandin E1 nor prostaglandin E2 inhibited the release of free fatty acids from the rabbit epigastric fat pad by ACTH1-24. 5. It seems likely that prostaglandin E2 is responsible for the vasodilatation accompanying fat mobilization from adipose tissue.

show abstract

“…Prostaglandin formation has been demonstrated in adipose tissue following nervous or hormonal stimulation (Shaw & Ramwell, 1968;Lewis & Matthews, 1970). The prostaglandin release associated with the vasodilatation accompanying lipolysis in rabbit was found to be prevented not only by prostaglandin synthetase inhibitors (Bowery & Lewis, 1973) but also by glucocorticoids (Lewis & Piper, 1975).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Glucocorticoids on the Distribution and Mobilisation of Arachidonic Acid in Fat Cell Ghosts

Lewis

Piper

Vigo

1979

British J Pharmacology

View full text Add to dashboard Cite

The prostaglandin synthesizing enzymes were found to be present in fat cell ghosts isolated from rabbit adipose tissue. Prostaglandin E2 (PGE2) and PGF2 were synthesized by ghosts after stimulation with adrenocor‐ticotrophic hormone (ACTH). Indomethacin was found to inhibit this synthesis but not the synthesis of lipoxygenase products. When fat cell ghosts were stimulated by ACTH, fatty acid release was observed from both neutral lipids and phospholipids. The arachidonic acid (AA) pool within the ghosts was identified: approximately 90% was present in the phospholipid fraction, 8.5% in the neutral lipids and 1.5% unbound. The glucocorticoids were found to stimulate incorporation of [14C]‐AA into neutral lipids and inhibit its incorporation into phospholipids. When fatty acid release was stimulated with ACTH, the glucocorticoids were found to inhibit the mobilisation of [14C]‐AA from the phospholipids and enhance its release from the neutral lipids. The glucocorticoids inhibit prostaglandin formation in fat cell ghosts.

show abstract

The mechanism of functional vasodilatation in rabbit epigastric adipose tissue

Cited by 31 publications

References 19 publications

Prostacyclin Production by Isolated Adipocytes

Prostacyclin Production by Isolated Adipocytes

The relationship between functional vasodilatation in adipose tissue and prostaglandin

The Effects of Glucocorticoids on the Distribution and Mobilisation of Arachidonic Acid in Fat Cell Ghosts

Contact Info

Product

Resources

About