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PubMed1988

Resistance vessel structure and function in the etiology of hypertension studied in F2-generation hypertensive-normotensive rats.

The role of certain resistance vessel characteristics in the etiology of hypertension has been investigated using F2-generation hypertensive/normotensive rats. The F2 populations were bred from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) as well as from stroke-prone SHR (SHRSP) and outbred Wistar-Kyoto rats (WKYO), and are denoted SHR/WKY and SHRSP/WKYO, respectively. Mesenteric resistance vessels (lumen diameter ca 200 micron) were taken from rats in the highest and lowest blood pressure quartiles of 14-week SHR/WKY and 18-week SHRSP/WKYO, as well as from 15-week pure SHR and WKY and from 18-week pure SHRSP and WKYO. The vessels were mounted on a myograph for determination of their structural and contractile characteristics. The structure of the vessels, as expressed for example by their media : lumen ratio, was greatest in the vessels from the SHR and the SHRSP compared to those from the WKY and WKYO. Increased structure was seen in the vessels from the rats in the high blood pressure quartiles of each group of F2 populations, compared to the vessels from the rats in the low blood pressure quartiles, although in the SHR/WKY the difference was smaller than expected if structure were a major determinant of blood pressure. Vascular sensitivity to calcium and the effect of cocaine on noradrenaline sensitivity were increased in the vessels from the SHR and SHRSP, but were the same in the high and low blood pressure quartiles of the F2 populations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Study of mechanisms of glucocorticoid hypertension in rats: endothelial related changes and their amelioration by dietary fish oils.

1. To investigate possible mechanisms of increased systolic blood pressure after 1 weeks treatment with dexamethasone and its amelioration by fish oil feeding, we have examined the reactivity of aortic rings and perfused mesenteric resistance vessels. 2. Thirty six Sprague-Dawley rats were initially divided into two groups and fed a semisynthetic diet containing either (10% by weight) hydrogenated coconut oil and safflower oil mixture (HCO/S) (24 rats) or fish oil (12 rats) for 5 weeks. From the end of the fourth week, dexamethasone (1.25 mg ml-1) in drinking water, was given to half the rats on hydrogenated coconut oil (HCO/S+Dex) and to the fish oil-fed group (fish oil+Dex). 3. One week of dexamethasone treatment raised systolic blood pressure in the HCO/S+Dex rats but not in the fish oil+Dex group. 4. Endothelium-dependent relaxation to acetylcholine (ACh) was decreased in aortic rings taken from HCO/S+Dex rats compared to rats on HCO/S alone. Relaxant responses to ACh of aortic rings from rats given fish oil+Dex were intermediate between the three groups. Aortic endothelium-independent responses to sodium nitroprusside (SNP) were unchanged between the groups, while aortic contractile responses to noradrenaline were similar in all the groups. 5. In the perfused mesenteric resistance artery, sensitivity to noradrenaline was decreased in rats given fish oil and dexamethasone compared to the other two groups. There were no differences in resistance vessel relaxation to ACh or SNP between groups. 6. Serum corticosterone levels, used as a marker of dexamethasone absorption, were substantially suppressed in dexamethasone-treated rats but levels were higher in rats on fish oil than on HCO/S diets. 7. We suggest that the glucocorticoid-induced rise in systolic blood pressure may be due in part to decreased aortic compliance as a consequence of impaired endothelium-dependent relaxation and perhaps reduced nitric oxide synthesis. Fish oil feeding may ameliorate this rise in blood pressure through (i) changes in dexamethasone absorption, (ii) decrease in reactivity to noradrenaline of perfused mesenteric resistance arteries, (iii) an increase in endothelium-dependent relaxation to ACh or a combination of these three factors.

6-Ketoprostaglandin F1 alpha↗

PubMed2004

Vasorelaxation induced by common edible tropical plant extracts in isolated rat aorta and mesenteric vascular bed.

In this study, the vasodilatory actions of nine edible tropical plant extracts were investigated. Ipomoea batatas (sweet potato leaf), Piper betle (betel leaf), Anacardium occidentale (cashew leaf), Gynandropsis gynandra (maman leaf), Carica papaya (papaya leaf), and Mentha arvensis (mint leaf) extracts exhibited more than 50% relaxing effect on aortic ring preparations, while Piper betle and Cymbopogon citratus (lemongrass stalk) showed comparable vasorelaxation on isolated perfused mesenteric artery preparation. The vascular effect on the aortic ring preparations were mainly endothelium-dependent, and mediated by nitric oxide (NO) as supported by the inhibition of action in the presence of N(omega)-nitro-L-arginine (NOLA), an nitric oxide synthase (NOS) inhibitor, or by the removal of endothelium. In contrast, vasodilatory actions in resistance vessels (perfused mesenteric vascular beds) appear to involve several biochemical mediators, including NO, prostanoids, and endothelium-dependent hyperpolarizing factors (EDHFs). Total phenolic contents and antioxidant capacities varied among different extracts and found to be independent of vascular relaxation effects. This study demonstrates that many edible plants common in Asian diets to possess potential health benefits, affording protection at the vascular endothelium level.

Animals↗

PubMed2001

Role of calcium channels in the spinal transmission of nociceptive information from the mesentery.

Opioids, alpha(2)-adrenoceptor agonists and blockers of voltage-gated calcium channels (VGCCs) have been attributed antinociceptive activity in various experimental set-ups. The present study tested the ability of morphine, clonidine and drugs acting at various VGCCs to inhibit the transmission of noxious stimuli from the mesentery at the level of the spinal cord. In rats under barbiturate anaesthesia traction of 20 g was applied to a bundle of mesenteric blood vessels. This caused immediate transient changes of mean arterial pressure that were taken as indication of nociception. Similar reflexes were elicited by applying 0.6% acetic acid to the same bundle of vessels. The reflexes were dose-dependently reduced by intrathecal administration of morphine or clonidine, but were left unaltered by intrathecal administration of verapamil, Bay-K 8644 or omega-conotoxin MVIIA. Neither verapamil nor Bay-K 8644 influenced clonidine-induced analgesia. Conotoxin markedly enhanced the effectiveness of all doses of clonidine against both types of mesenteric stimuli. Verapamil, Bay-K 8644, as well as conotoxin reduced the ability of morphine to inhibit mechanically evoked reflexes, while there was no statistically significant effect in chemonociception. These data suggest that, at the spinal level, both morphine and clonidine are effective drugs to decrease the cardiovascular changes caused by acute mesenteric pain. In the dorsal spinal cord neither L-type nor N-type VGCCs are responsible on their own for the transmission of noxious stimuli from the mesentery. Inhibition of N-type channels markedly augments the action of clonidine, whereas blocking either VGCC seems to inhibit antinociceptive mechanisms induced by morphine. It is suggested that in patients the combined administration of clonidine with omega-conotoxin MVIIA might lead to effective pain control with reduced side effects.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1982

The morphology of canine lymphatic valves.

The architecture of 60 valves from thoracic ducts and from renal hilar and mesenteric collecting lymph vessels of dogs were studied by scanning electron microscopy as well as by light and transmission electron microscopy. All of the valves seen in hilar and mesenteric lymph vessels and most of those studied in the thoracic duct were bicuspid. An occasional tricuspid and one monocuspid valve was seen in the thoracic duct. The semilunar cusps of the valves extended from the vessel wall, to which they were attached, towards the valve outlet where adjacent cusps fused. Coincident to the area of fusion was the formation of mesenteric-like folds or buttresses that anchored the cusps to the vessel wall. These folds extended 50-100 micrometers beyond the cusp margins on the outflow side of the valve. The attachments of the cusps, buttresses, and vessel wall to one another resulted in the formation of postvalvular sinuses, such that raised intraluminal pressure downstream to valve areas would distend the sinuses, causing leaflet apposition and hence valvular closure. The morphology of the valves was such that they were not considered to provide any significant impediment to the antegrade flow of lymph.

Animals↗

PubMed1987

Effect of phenylephrine and isoproterenol on mesenteric blood flow in experimental posthaemorrhagic hypotension.

In previous reports it was found that in mesenteric blood vessels exist profound alpha-adrenergic, and less profound beta-adrenergic receptors. Our experiments were done on 20 mongrel dogs, both sexes, weighing 6.5-22.5 kg, age from 1-2 years, which were divided into 2 groups: experimental (14 dogs) and control (6 dogs). Experimental group of animals passed through the posthemorrhagic hypotension (180 min. at 5.3 kPa). Aim of investigation was to clarify mesenteric vascular reactivity changes during posthemorrhagic hypotension. In order to reach this goal, phenylephrine and isoproterenol were injected alternatively in one hour intervals through cannulated superior mesenteric artery first proximal branch. Our results indicate that mesenteric blood flow responses to those drugs changed quantitatively, but never ceased. It is apparent from our experiments that those quantitative changes are due to beta 2 adrenoceptors changes during the posthemorrhagic hypotension.

Animals↗

PubMed1991

Electrophysiological studies on the interaction of 5-hydroxytryptamine with sympathetic transmission in the guinea pig inferior mesenteric artery and ganglion.

The interaction of 5-hydroxytryptamine (5-HT) with sympathetic transmission was investigated in the guinea pig inferior mesenteric artery (IMA) and ganglion (IMG). Intracellular recordings of membrane potential were made using glass microelectrodes. Superfusion of 5-HT (0.3 microM) reduced the amplitudes of stimulation-evoked excitatory junction potentials in the IMA. 5-HT had no effect on depolarizing responses to pressure-ejection of adenosine triphosphate or norepinephrine in the IMA. The inhibitory effect of 5-HT on excitatory junction potentials in the IMA was abolished by methysergide (3 microM), but was unaffected by the following antagonists: methiothepin (1 microM), MDL 72222 (3 microM), MDL 11939 (0.3 microM) or by phentolamine (10 microM). In the IMG, pressure-ejection of 5-HT (10 mM) evoked fast and slow depolarizing responses in 77% of neurons tested; the fast depolarizing responses to 5-HT were reduced in the presence of MDL 72222 (5 microM). Superfusion of 5-HT (0.3-3 microM) had no effect on stimulation-evoked fast excitatory postsynaptic potentials in the IMG. Thus, the results of the present study suggest that, depending on its site of interaction with postganglionic sympathetic neurons, 5-HT may have excitatory or inhibitory effects on sympathetic transmission. 5-HT may inhibit transmitter release through the activation of as yet unidentified 5-HT receptors on the sympathetic nerve endings in mesenteric blood vessels. Whereas, in the prevertebral ganglion, 5-HT may act to facilitate sympathetic transmission, in part, through activation of 5-HT3, receptors on the somata of principal neurons.

Animals↗

PubMed1994

Characterization of contractile properties of porcine mesenteric and tracheobronchial lymphatic smooth muscle.

We performed morphometric and length-tension analyses comparing mesenteric and tracheobronchial lymph vessel segments to determine the potential of the latter tissue to regulate pulmonary and mediastinal lymph flow via alterations in smooth muscle tone. Fresh porcine lymph vessel rings were prepared for 1) in vitro assessment of length-tension relationships and 2) histologic preparation and measurement of smooth muscle cross-sectional area (SMA). Mesenteric and tracheobronchial optimal vessel ring lengths were 3.1 +/- 0.2 and 3.5 +/- 0.2 mm, and maximum active tensions were 1518 +/- 25 and 1703 +/- 162 mg. Smooth muscle formed indistinct layers in each tissue, and only 30% of the smooth muscle was oriented circumferentially. Stress generated by the circular smooth muscle was similar to that generated by other types of vascular smooth muscle. In 75% of mesenteric vessel rings spontaneous contractions were observed that had a mean contraction frequency of 1.7 +/- 0.2 min-1 and a mean contraction amplitude of 349 +/- 35 mg, while only 40% of tracheobronchial vessels exhibited spontaneous contractions (p < 0.001) that had a mean frequency of 0.6 +/- 0.2 min-1 (p = 0.0021) and a mean contraction amplitude of 118 +/- 10 mg (p < 0.0001). We conclude that tracheobronchial lymphatic vascular smooth muscle is capable of developing stress similar to that generated by mesenteric lymph vessels, and that spontaneous rhythmic contractile activity is qualitatively and quantitatively different in tracheobronchial than in mesenteric porcine lymph vessels. The data suggest that tracheobronchial lymph vessels are capable of regulating pulmonary and mediastinal lymph flow through intrinsic mechanisms. Such regulation may occur by alterations in vascular resistance rather than via spontaneous pumping activity.

Animals↗

PubMed1995

Characterisation of angiotensin converting enzyme from different rat vascular beds.

The tissue renin angiotensin system may play a role in cardiovascular pathophysiology. Angiotensin converting enzyme in tissues is now a target for pharmacological inhibition. It is therefore important to determine whether ACE is evenly distributed throughout the vascular tree and whether the enzyme has the same characteristics in different vascular beds. We have thus measured angiotensin converting enzyme density in three functionally different vascular beds with three different methods: the enzyme kinetic assay, a radioligand binding assay and in vitro autoradiography. All three methods demonstrated a significantly higher binding density and activity of ACE in resistance arteries from the mesenteric vascular bed of rats than in microvessels from the brain, or in a conduit artery, the aorta. The dissociation constant (Kd) of the enzyme-radioligand complex was the same in the three functionally different vessel types. Radioligand displacement studies for ACE from plasma and the mesenteric vessels in vitro utilizing a panel of different ACE inhibitors have shown a similar rank order of inhibitory potency suggesting that catalytic sites of ACE were the same in plasma and the mesenteric microvessels. In vivo, the enzyme inhibition in plasma, mesenteric and brain vessels measured by enzyme kinetic and radioligand binding assay were well correlated. There was a similar degree of inhibition between different vessels and tissues (mesenteric vessels, aorta, kidney, left ventricle and coronaries) measured by in vitro autoradiography.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1975

Cardiovascular pharmacology of bombesin, a new polypeptide from amphibian skin.

Bombesin is a tetradecapeptide extracted from the side of discoglossid frogs Bombina bombina and Bombina variegata variegata. In anaesthetized dogs bombesin causes mainly systemic hypertension, bradycardia and constriction of the renal, mesenteric and coeliac arterial vessels. The other vascular beds studied (carotid, femoral and coronaric) passively follow the blood pressure. Tachyphylaxis may occur. Dibenzyline and hexamethonium do not antagonize the hypertensive property of bombesin, while the occlusion either of the renal vessels or of the mesenteric, coeliac arteries and portal vein reduces the intensity and the duration of the hypertensive response. The simultaneous occlusion of all the above mentioned vessels further reduces the duration of the hypertensive response evoked by bombesin and reverses its effect on the heart from mainly bradycardic to pure tachycardic. In these condition bombesin causes carotid and peripheral vasoconstriction. The increase of heart rate and of blood pressure, while occurs after ligation of aplanchnic vessels, is completely or partly antagonized by propranolol. In normal conscious dogs bombesin is at least 10 times more potent and less tachyphylactic than in anesthetized dogs.

Amphibians↗

PubMed1984

Resistance vessel abnormalities in spontaneously hypertensive rats.

This paper summarizes and discusses investigations in the author's laboratory designed to determine whether certain cardiovascular parameters which differ in 12- to 14-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY) are associated with the cause of the difference in the blood pressures of these animals. The investigations include age studies, antihypertensive-treatment studies, studies of hybrid SHR/WKY, as well as studies of renal hypertensive and of normotensive Wistar rats. The parameters studied include heart/body-weight ratio and the media/lumen ratio and calcium sensitivity of the norepinephrine response of mesenteric resistance vessels (internal diameter 150-200 micron). The results indicate that heart/body-weight ratio and media/lumen ratio of resistance vessels are increased in 12- to 14-week-old SHR and suggest that this is due primarily to genetic factors rather than to the increased blood pressure. Furthermore, these structural abnormalities do not appear to be a sufficient cause of the increased blood pressure. On the other hand, the calcium sensitivity of the resistance vessels, which is also increased in SHR, may be associated with the genetic factors responsible for the increased blood pressure.

Aging↗

PubMed1980

Characteristics of prostaglandin E1 potentiation of inflammatory activity of some agents.

In rats pretreated with indomethacin, injection of PGE1 (prostaglandin E1) with carrageenan potentiated the carrageenan paw oedema. This effect of PGE1, was maximal when it was injected together with carrageenan, there being a reduction in the action of PGE1 if carrageenan injection was delayed after PGE1 injection. PGE1 induced potentiation of increase in plasma protein leakage induced by intradermal injections of bradykinin and histamine also depended on the injection of PGE1 along with these agents. Thus oedema enhancement by PGE1 differs from its action in pain, where PGs cause a long lasting sensitization of the injected area for the actions of other algesics. Since vasodilation may be a mechanism of oedema enhancement by PGs, the ability of adenosine and papaverine to mimic PGE1 in paws and skins of rats were examined. Adenosine was active whereas papaverine was inactive in this respect. To clarify this difference, the vasodilatory properties of PGE1, adenosine and papaverine were assessed by their ability to antagonize NA response in perfused rat mesenteric blood vessels. Only papaverine was effective in antagonising the NA response. Thus, PGE1 and adenosine which potentiated the oedema inducing actions of other agents showed no vasodilatory properties and papaverine, a vasodilator, had no oedema potentiating actions.

Adenosine↗

PubMed1999

Peripheral projections of primary sensory neurons immunoreactive for brain-derived neurotrophic factor.

Brain-derived neurotrophic factor (BDNF) is synthesized in a subpopulation of primary sensory neurons and transported anterogradely to the spinal cord and peripheral targets. In the present study, the peripheral projection of sensory neurons immunoreactive (-ir) for BDNF was examined by a combined method of immunohistochemistry and retrograde tracing in rats. It was found that 36.3% of sensory neurons projecting to subcutaneous tissues, 9.8% to epidermis and 8.3% to muscle, contained BDNF immunoreactivity. In contrast, only 0.2% of sensory neurons projecting to adrenal gland and 0.9% to coeliac ganglia contained BDNF. A small proportion of sensory neurons projecting to muscles, mesenteric blood vessels and hair follicles was also BDNF immunoreactive. These results provide evidence that primary sensory neurons immunoreactive for BDNF project mainly to subcutaneous tissues but not to autonomic ganglia and their adjacent viscera.

Animals↗

PubMed2003

Characterization of angiotensin-(1-7) receptor subtype in mesenteric arteries.

Mesenteric arteries from male Sprague-Dawley rats were mounted in a pressurized myograph system. Ang-(1-7) concentration-dependent responses were determined in arteries preconstricted with endothelin-1 (10(-7)M). The receptor(s) mediating the Ang-(1-7) evoked dilation were investigated by pretreating the mesenteric arteries with specific antagonists of Ang-(1-7), AT(1) or AT(2) receptors. The effects of Ang-(3-8) and Ang-(3-7) were also determined. Ang-(1-7) caused a concentration-dependent dilation (EC(50): 0.95 nM) that was blocked by the selective Ang-(1-7) receptor antagonist D-[Ala(7)]-Ang-(1-7). Administration of a specific antagonist to the AT(2) receptor (PD123319) had no effect. On the other hand, losartan and CV-11974 attenuated the Ang-(1-7) effect. These results demonstrate that Ang-(1-7) elicits potent dilation of mesenteric resistance vessels mediated by a D-[Ala(7)]-Ang-(1-7) sensitive site that is also sensitive to losartan and CV-11974.

Angiotensin I↗

PubMed2003

Mechanotransduction via the elastin-laminin receptor (ELR) in resistance arteries.

The arterial wall is composed of dynamically interacting cellular and acellular components that are necessary for the maintenance of vessel homeostasis. Two extracellular proteins in the vessel wall, elastin and laminin, play important structural roles. We recently established a role for the elastin-laminin receptor (ELR) in mechanotransduction of stretch in cultured vascular smooth muscle (VSM) (Am. J. Physiol.: Heart Circ. Physiol. 280(3) (2001) H1354). We found stretch-mediated signaling by the ELR decreased the expression of the proto-oncogene, c-fos, and subsequent cellular proliferation. However, the role for the ELR in mediating pressure-induced changes in gene expression in intact, isolated resistance vessels is unknown and the goal of this study was to ascertain this possibility. In this study, isolated rat cerebral (approximately 180 microm) and mesenteric (approximately 280 microm) arteries were pressurized to 65 mmHg (baseline) and this pressure was held for 2 h. After this equilibration, pressures were increased to either 80 mmHg (n=6) or 140 mmHg (n=6) for 30 min and transcript levels of c-fos and the housekeeping gene, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA were assessed by reverse transcriptase-polymerase chain reaction (RT-PCR). Elevation of pressure in the cerebral arteries decreased the c-fos/GAPDH ratio by 72% in the 140 mmHg group compared to the 80 mmHg control. Importantly, the decrease in c-fos expression was blocked by ELR peptide antagonists (VGVAPG or YIGSR, 10 microM, n=6). In contrast, the decrease in c-fos expression was not observed in the mesenteric resistance arteries. In these vessels, pressure (140 mmHg) increased the c-fos/GAPDH ratio (+68% compared to normotensive control, n=6). To account for the difference between the cerebral and mesenteric vessels, histological analysis of elastin fiber content was performed. Cerebral arteries have greater amounts of loose elastin fibers (fibers outside of the organized elastin laminae) in the tunica media compared to mesenteric arteries. This may explain the opposite stretch-induced responses of c-fos expression in these vessels. Stretch-induced ELR signaling may play a prominent role in vascular adaptations to hypertension in specific organ systems. Our data further suggest that ELR activation may represent a larger component of mechanosensitive signaling in the cerebral circulation than in the mesenteric circulation.

Animals↗

PubMed2000

Effect of somatostatin on resistance and on capacitance rabbit isolated arteries.

The effects of somatostatin, a tetradecapeptide isolated from hypothalamus extracts, were studied on the vascular reactivity of aorta and mesenteric arteries isolated from rabbits. We also investigated whether or not Ca(2+) movements were implicated in these effects. Rabbit aorta and mesenteric (fifth branch) arteries were isolated, cleaned off, and mounted in an organ bath containing Godfraind solution or physiological saline solution (PSS), respectively. Somatostatin (10(-8)-10(-4) M) produced a concentration-dependent inhibition of the contractile responses induced by high K(+) (80 mM) or noradrenaline (10(-6) M in aorta or 10(-4) M in mesenteric arteries) in both arteries studied. The inhibitory effect of somatostatin was greater in mesenteric resistance vessels (IC(50) 3.1+/-2.3x10(-5) M, and 5.2+/-4.8x10(-8) M with KCl and noradrenaline, respectively). Contractile responses produced by the addition of Ca(2+) (1-5 mM) to Ca(2+)-free high K(+) solution were also concentration dependently inhibited by somatostatin in aorta. Furthermore, somatostatin decreased noradrenaline-induced contraction attributed to intracellular Ca(2+) release in aorta, and inhibited 45Ca(2+) uptake stimulated by high K(+) or by noradrenaline. However, it did not modify 45Ca(2+) uptake in resting mesenteric resistance arteries. Taken together, these results suggest that somatostatin exerts an inhibitory effect on vascular contractions induced by some stimulating agents in different arteries isolated from rabbits, being more potent in mesenteric arteries.

Animals↗

PubMed1991

Cromakalim inhibits contractions of the rat isolated mesenteric bed induced by noradrenaline but not caffeine in Ca(2+)-free medium: evidence for interference with receptor-mediated Ca2+ mobilization.

The effects of the K+ channel opener cromakalim on phasic contractions induced by noradrenaline and caffeine were studied in the rat isolated mesenteric bed. In the presence of 1.4 mM Ca2+, 1-s pulses of noradrenaline increased the perfusion pressure of the preparation concentration dependently (midpoint at 92 +/- 10 microM noradrenaline). Cromakalim (0.3 and 1 microM) inhibited these contractions in a non-competitive manner. Contractions elicited by 1-s pulses of noradrenaline (100 microM) were inhibited by the dihydropyridine Ca2+ antagonist isradipine by maximally 24 +/- 1%, indicating that only a minor component of this contraction depended on Ca2+ entry via dihydropyridine-sensitive Ca2+ channels. Cromakalim was a much more effective inhibitor of these contractions (maximum inhibition by 80%, midpoint of the inhibition curve at 171 +/- 15 nM). The effect of cromakalim was stereoselective, inhibited by the sulphonylurea glibenclamide, and abolished in partially depolarizing media (KCl = 35 and 50 mM). In Ca(2+)-free medium, cromakalim inhibited the contraction induced by noradrenaline (100 microM) by maximally 69 +/- 4%, with a midpoint at 58 +/- 14 nM. The effect of cromakalim was again stereoselective, inhibited by glibenclamide, and abolished in the presence of 50 mM KCl. Contractions induced by caffeine (10 and 100 microM) were not affected by cromakalim (1 microM). The results indicate that, in rat mesenteric resistance vessels, cromakalim interferes with the ability of noradrenaline, but not caffeine, to mobilize Ca2+ from intracellular stores. The antivasoconstrictor effect of cromakalim against noradrenaline is inhibited by glibenclamide and appears to be linked to the ability of cromakalim to hyperpolarize the cell membrane.

Animals↗

PubMed1983

Intestinal vascular responses to dopamine during fentanyl-nitrous oxide anaesthesia, supplemented with dixyrazin.

Intestinal haemodynamics in response to continuous i.v. administration of dopamine were investigated in cats anaesthetized with fentanyl-nitrous oxide either with or without supplement of dixyrazin. A dose-dependent vasodilatation was observed in the dopamine dose range 2.5-35 micrograms . kg-1 . min-1 and the subsequent maximal intestinal blood flow increase was 121%. No net intestinal vasoconstriction was evident even at the largest dopamine doses, although the vascular response reached a plateau at 17.5 micrograms . kg-1 . min-1. Control experiments during chloralose anaesthesia gave similar results. Changes in mean arterial pressure and heart rate were small. Renal blood flow was virtually unchanged at dopamine doses below 10 micrograms . kg-1 . min-1, while renal vasoconstriction was evident following dopamine doses above that level. The addition of i.v. dixyrazin (0.15-0.30 mg . kg-1) to the fentanyl-nitrous oxide anaesthesia substantially potentiated the intestinal vasodilator response to i.v. dopamine and the maximal blood flow increase was 183% at 10-15 micrograms . kg-1 . min-1. In vitro experiments using mesenteric resistance vessels from the rat demonstrated a dose-dependent relaxation to dopamine. At very large doses this response was counteracted, but not reversed into vasoconstriction by dopamine-induced alpha-adrenergic stimulation.

Animals↗