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PubMed2005

Phase resetting of arterial vasomotion by burst stimulation of perivascular nerves.

Arteries display cyclic diameter variations, vasomotion. In vivo, these rhythmic contractions are modulated by the influence of sympathetic nerves. In this study, we investigated the effect of burst stimulation of intramural nerves in vitro on the vasomotion of rat mesenteric small arteries. Vessels were mounted for isometric force measurement. After initiation of vasomotion with noradrenaline (0.5-2 microM), periarterial sympathetic nerves were stimulated electrically (10 impulses at 20 Hz) at approximately half-minute intervals. With a delay of 2-3 s, a neurogenic burst caused a brief contraction of the vascular smooth muscle and altered the period of the current vasomotion cycle. The effect on amplitude decayed rapidly and was practically not apparent in the next vasomotion cycle after the burst. With respect to period, stimulation at increasing intervals from the trough in force of vasomotion caused gradual prolongation of the cycle until a critical interval was reached, after which cycle duration was reduced instead. Since subsequent cycles were not affected, a change in phase remained. When two segments of oscillating arteries were mounted in a two-vessel myograph, simultaneously applied bursts of impulses synchronized their oscillation. The data suggest that changes in neural activity are able to make different vessels oscillate in phase, thereby coordinating vasomotion in different parts of the vascular tree, possibly explaining the synchronicity of vasomotion in different vascular beds that can be observed in vivo.

Animals↗
PubMed1982

Kininases and vascular responses to kinins.

We have utilized several inhibitors to assess the effects of kininases on the contractile activity of bradykinin (BK), kallidin (KD), des-Arg9-BK and des-Arg10-KD on two isolated blood vessels, the rabbit aorta and mesenteric vein. The response of the two vessels to kinins are mediated by B1-receptors, implying that fragments of kinins without the C-terminal arginine are much more active on these tissues than the whole kinin sequences. Blockers of carboxypeptidase B-like enzymes, such as SQ24798 and pivalyl-L-arginine decrease the apparent affinity of BK and KD on the two vessels, while not changing those of des-Arg9-BK and des-Arg10-KD; this suggests that a major part of the contractile activities of BK and KD are mediated by des-Arg metabolites formed in situ at the tissue level by a kininase I. The block of kininase II by captopril or desacetylated MK-421 bring about a complex pattern of activity changes that include the potentiation of BK and KD and the depression of des-Arg10-KD. These results, in conjunction with those obtained with the non-specific inhibitors of metallopeptidases, thioglycolic acid and EDTA, suggest that the relative contribution of kininase I and kininase II to the degradation of kinins in arterial and venous vessels may be different. The implications of these findings on the pharmacology of B1-receptors are discussed.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Atherosclerosis of the visceral arteries.

Thrombosis in the visceral arteries is the most common cause of acute mesenteric ischemia. It typically occurs in areas of atherosclerotic narrowing. Atherosclerosis of splanchnic blood vessels also causes chronic mesenteric ischemia. In the present study, the occurrence of atherosclerosis in the celiac and mesenteric arteries was evaluated in an unselected Finnish autopsy series of 120 patients. Thirty-five patients (29%) had stenosis in the first few centimetres of mesenteric arteries. In 18 cases (15%) at least two mesenteric arteries were stenotic. The celiac artery was the most common site of mesenteric artery stenosis. More distally, only hemodynamically insignificant signs of macroscopic atherosclerosis, fatty streaks or fibrous plaques, observed. The occurrence of mesenteric artery stenosis was strongly associated with aging. Sixty-seven per cent of the subjects aged 80 or more presented with mesenteric artery stenosis, whereas the rate was 6% among those aged less than 40 years. Despite sometimes extensive stenotic alterations in the mesenteric arteries, only one patient in our study had bowel necrosis at autopsy. We conclude that atherosclerosis of mesenteric arteries commonly affects individuals of advanced age. As a part of general arteriosclerotic process of the circulatory system, mesenteric artery atherosclerosis is strongly associated with atherosclerosis in coronary arteries. In addition, there was an association between atherosclerosis in mesenteric arteries and cerebral arteries in the skull base. Thus, a characteristic triad of postprandial abdominal pain, food aversion, and weight loss in an elderly patient with other manifestations of arteriosclerosis should suggest a possibility of the visceral arterial insufficiency.

Adult↗
PubMed1989

Different involvement of endothelium-derived relaxing factor and prostacyclin in vasodilator response to bradykinin in isolated dog blood vessels.

The study presented so far demonstrates that there is a heterogeneity in the mechanisms of vasodilator action of BK in various dog blood vessels (coronary vs mesenteric artery, and mesenteric artery vs vein). The different mechanisms underlying the BK-induced vasodilatation are summarized in Fig. 3. Three mechanisms are at least involved; 1) EDRF-release from endothelial cells which may not be mediated by B1 receptor, but presumably by B2 receptor, 2) PGI2-release from endothelial cells, 3) PGI2-release from smooth muscle (subendothelial) cells. The PGI2-release may be mediated by B1 receptor. Vasodilatation caused by BK is mediated via "1" in coronary arteries, "2" + "3" in mesenteric veins, and "1" + "2" + "3" in mesenteric and renal arteries in the dog. Another reasons for the differences in the BK-induced vasodilatation may be different number or sensitivity of BK receptors located on the endothelial and smooth muscle cells, or the responsiveness of the vascular smooth muscle cells to the intermediate vasodilator substances and BK itself.

Animals↗
PubMed1986

[Application of NMR-CT in the staging of cancer of the digestive organs].

To assess the potential of NMR-CT for demonstrating cancer of the digestive organs, we examined a total of 232 patients (89 with esophageal cancer, 52 with liver cancer, 40 with colorectal cancer, 9 with pancreatic cancer, 9 with gastric cancer, and 33 with other diseases). NMR-CT has many features, but we use especially those features which it is possible to select not only in the transverse plane but also in the coronal and sagittal planes, and it has excellent soft tissue contrast resolution. Our machine is a Picker International NMR-CT using a superconducting magnet of 0.256 tesla. Diagnosis of lymph node involvement of esophageal cancer. Using only the coronal plane, each patient was scanned by the spin echo technique (TE = 40, TR = 400) from the plane of the descending aorta to the plane of the trachea 1 cm in thickness, at 1 cm intervals, continuously. All the vessels were clearly differentiated as no-signal regions, especially in coronal images, from areas of carcinomatous involvement. Lymph nodes were identified as intense grey masses in fat tissue of high intensity. Twenty cases were proved by surgery or autopsy, and it was possible to assess 160 lymph-node groups. A total of 25 patients were imaged as having positive lymph nodes, but 17 of them had metastasis-positive nodes. In other 135 nodes imaged as negative lymph nodes, only two had metastasis and 133 were negative for metastasis. Overall accuracy was 93.8%. Diagnosis of liver cancer. Intrahepatic vessels were clearly imaged without using contrast enhancement in NMR-CT, so it was easy to diagnose the segment containing the tumor and to detect tumor emboli in the portal vein. The capsule was imaged in 84% (16/19) using IR techniques, although only 37% (7/19) could be imaged by X-CT. Diagnosis of colorectal cancer. Using the sagittal plane, the sacrum, urinary bladder and other organs were imaged better parallel to their axis, so that the relationship between rectal cancer and surrounding organs could be clearly visualised with NMR-CT. With regard to lymphatic metastasis, coronal imaging was useful for picturing mesenteric and pelvic vessels, so that lymph nodes were imaged as low-intensity masses along the vessels. Lymph metastasis almost 1 cm size can be detected using coronal NMR-CT.

Digestive System Neoplasms↗
PubMed2004

Irreversible lower limb ischaemia following ligation of the inferior mesenteric artery in the surgical treatment of rectal cancer.

Rectal cancer and cardiovascular disease are both commoner in the elderly and may coexist. In some severe arteriopaths the blood supply to the lower limbs may be a collateral circulation from the inferior mesenteric artery. Patients with aorto-iliac occlusion or severe stenosis may have collaterals from the inferior mesenteric artery to the lower limb blood vessels. Ligation of the inferior mesenteric artery in treating rectal cancer can result in irreversible ischaemia as outlined in this report. Routine palpation of the femoral pulses and awareness of collateral circulation may avoid the disastrous consequences seen in the two cases described.

Aged↗
PubMed2006

Microvascular versus macrovascular dysfunction in type 2 diabetes: differences in contractile responses to endothelin-1.

Vascular dysfunction characterized by a hyperreactivity to vasoconstrictors and/or impaired vascular relaxation contributes to increased incidence of cardiovascular disease in diabetes. Endothelin (ET)-1, a potent vasoconstrictor, is chronically elevated in diabetes. However, the role of ET-1 in resistance versus larger vessel function in mild diabetes remains unknown. Accordingly, this study investigated vascular function of third-order mesenteric arteries and basilar arteries in control Wistar and Goto-Kakizaki (GK) rats, a model of mild Type 2 diabetes. Six weeks after the onset of diabetes, contractile responses to 0.1-100 nM ET-1 and relaxation responses to 1 nM-10 microM acetylcholine (ACh) in vessels preconstricted (baseline + 60%) with serotonin (5-HT) were assessed by myograph studies in the presence or absence of a nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine (L-NNA). Maximum contractile response to ET-1 was augmented in mesenteric vessels (155 +/- 18% in GK vs. 81 +/- 6% in control; n = 5-7) but not in the basilar artery (134 +/- 29% in GK vs. 107 +/- 17% in control; n = 4 per group). However, vascular relaxation was impaired in the basilar arteries (22 +/- 4% in GK vs. 53 +/- 7% in control; n = 4 per group) but not in mesenteric arteries of GK rats. Inhibition of NOS decreased the relaxation response of basilar arteries to 15 +/- 8% and 42 +/- 5% in GK and control rats, respectively; whereas, in resistance vessels, corresponding values were 56 +/- 7% and 89 +/- 3% (vs. 109 +/- 2% and 112 +/- 3% without NOS blockade), indicating the involvement of different vasorelaxation-promoting pathways in these vascular beds. These findings provide evidence that the ET system is activated even under mild hyperglycemia and that it contributes to the hyperreactivity of resistance vessels, therefore, the ET system may play an important role in elevated blood pressure in Type 2 diabetes.

Acetylcholine↗
PubMedDate not supplied

Prolonged exposure to ouabain eliminates the greater norepinephrine-dependent calcium sensitivity of resistance vessels in spontaneously hypertensive rats.

The effects of 30 minutes of exposure to ouabain on calcium sensitivity have been investigated in two types of resistance vessels from 12 pairs of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Branches of the superior mesenteric and femoral arteries, with internal diameters of about 200 micrometer, were mounted as ring preparations in a myograph capable of measuring their isometric wall tension. Dose-response curves for calcium upon norepinephrine stimulation were determined under conditions where neuronal uptake was eliminated. Initially, when stimulated with norepinephrine, the SHR vessels from both locations were more sensitive to calcium and had stronger contractions than their controls. The addition of ouabain (1 mM) to the relaxed vessels immediately elicited a moderate, transient contraction in the branches of the femoral artery, whereas no response was observed in the mesenteric vessels. Although the addition of ouabain to activated vessels produced an immediate potentiation of the response, prolonged (30-minute) exposure to ouabain reduced active tension development upon norepinephrine stimulation in all vessels. The reduction was greatest in the SHR vessels, so that, under these conditions, the norepinephrine-activated calcium sensitivity of corresponding SHR and WKY vessels was similar. By contrast, responses to norepinephrine in high potassium solution were unaffected. The results suggest that under normal conditions, SHR vessels may have a specific increase in the permeability of the norepinephrine-activated calcium channels. Prolonged exposure to ouabain appears to reduce the permeability of these channels, providing an explanation for why this treatment eliminates the difference in calcium sensitivity of the SHR and WKY vessels.

Animals↗
PubMed1978

Gastrointestinal angiographic findings in systemic amyloidosis.

Amyloidosis is a multisystem disease process of unknown cause in which characteristically staining protein-polysaccharide material is deposited in body tissues. Although gastrointestinal involvement is usually asymptomatic, amyloid infiltration of mesenteric and submucosal vessel walls may be associated with acute or recurrent gastrointestinal hemorrhage in patients with the diagnosis of amyloidosis. Angiography in such cases may demonstrate arterial and venous changes as a result of these vascular wall deposits. Two patients with proven amyloidosis and gastrointestinal hemorrhage are presented, and their angiographic findings are discussed with the pathologic correlations.

Amyloidosis↗
PubMed1976

Adrenergic neuronal degeneration induced in portal vein and caudal artery by 6-hydroxydopamine in vitro.

Fluorescence histochemistry and electron microscopy were used to study the structural consequences of in vitro exposure to the sympatholytic agent 6-hydroxydopamine on two blood vessels, the portal mesenteric vein and caudal artery of the rat. The results showed depletion of catecholamines to indetectable levels associated with clear signs of adrenergic nerve degeneration, such as cytoplasmic shrinking, virtual absence of dense core vesicles and swelling of mitochondria. All of the changes observed occurred within 2 hours in the caudal arteries and 3.5 hours in the portal veins. Comparison of electron and fluorescence micrographs of incubated control specimens with those of unincubated, fresh specimens showed that the nerve endings of the incubated controls were well preserved for at least 3.5 hours. With destruction of nerve endings in such a short period of time, the processes of specific neuronal degeneration could be clearly demonstrated in isolated blood vessels.

Animals↗
PubMed2001

Mechanisms of isoflurane-mediated hyperpolarization of vascular smooth muscle in chronically hypertensive and normotensive conditions.

BACKGROUND: The purpose of this study was to compare the effects of isoflurane on membrane and intracellular mechanisms that regulate vascular smooth muscle (VSM) transmembrane potential (Em; which is related to VSM tone) in the spontaneously hypertensive rat (SHR) model of essential hypertension and its normotensive Wistar-Kyoto (WKY) control. METHODS: Vascular smooth muscle Em values were measured in situ in locally denervated, superfused, intact, small (200-300-microm OD) mesenteric arteries and veins in anesthetized 9-12-week-old SHR and WKY. Effects of 1.0 minimum alveolar concentration (0.60 mM) superfused isoflurane on VSM Em were measured before and during superfusion with specific inhibitors of VSM calcium-activated (KCa) and adenosine triphosphate-regulated (KATP) potassium channels, and with endogenous mediators of vasodilatation (nitric oxide, cyclic guanosine monophosphate, protein kinase G, cyclic adenosine monophosphate, and protein kinase A). RESULTS: Isoflurane significantly hyperpolarized small arteries (5 +/- 3.4 mV) and veins (6 +/- 4.7 mV) (pooled SHR and WKY, mean +/- SD). Inhibition of KCa and KATP channels, cyclic adenosine monophosphate, and protein kinase A, but not nitric oxide, cyclic guanosine monophosphate, and protein kinase G, abolished such hyperpolarization equally in SHR and WKY vessels. CONCLUSIONS: Isoflurane-induced in situ VSM hyperpolarization in denervated, small mesenteric vessels involves a similar activation of KCa and KATP channels and cyclic adenosine monophosphate, but not nitric oxide or cyclic guanosine monophosphate, second messenger pathways in both SHR and WKY. A greater isoflurane-induced VSM hyperpolarization (observed previously in neurally intact SHR vessels) suggests enhanced inhibition of elevated sympathetic neural input as a major mechanism underlying such hyperpolarization (and coupled relaxation) in this neurogenic model of hypertension.

Anesthetics, Inhalation↗
PubMed1995

Specificity of different organic nitrates to elicit NO formation in rabbit vascular tissues and organs in vivo.

1. In the present study we assessed the formation of nitric oxide (NO) from classical and thiol-containing organic nitrates in vascular tissues and organs of anaesthetized rabbits, and established a relationship between the relaxant response elicited by nitroglycerin (NTG) and NO formation in the rabbit isolated aorta. Furthermore, the effect of isolated cytochrome P450 on NO formation from organic nitrates was investigated. 2. Rabbits received diethyldithiocarbamate (DETC; 200 mg kg-1 initial bolus i.p. and 200 mg kg-1 during 20 min, i.v.) and either saline, or one of the following organic nitrates: nitroglycerin (NTG, 0.5 mg kg-1), isosorbide dinitrate (ISDN), N-(3-nitratopivaloyl)-L-cysteine ethylester (SPM 3672), S-carboxyethyl-N-(3-nitratopivaloyl)-L-cysteine ethylester (SPM 5185), at 10 mg kg-1 each. After 20 min the animals were killed, blood vessels and organs were removed, and subsequently analyzed for spin-trapped NO by cryogenic electron spin resonance (e.s.r.) spectroscopy. 3. In the saline-treated control group, NO remained below the detection limit in all vessels and organs. In contrast, all of the nitrates tested elicited measurable NO formation, which was higher in organs (liver, kidney, heart, lung, spleen) (up to 4.8 nmol g-1 20 min-1) than in blood vessels (vena cava, mesenteric bed, femoral artery, aorta) (up to 0.7 nmol g-1 20 min-1). Classical organic nitrates (NTG, ISDN) formed NO preferentially in the mesenteric bed and the vena cava, while the SPM compounds elicited comparable NO formation in veins and arteries. 4. Using a similar spin trapping technique, NO formation was assessed in vitro in phenylephrine-precontracted rabbit aortic rings. The maximal relaxation elicited by a first exposure (10 min) to NTG (0.3 to 10 microM) was positively correlated (r = 0.8) with the net increase (NTG minus basal) of NO spin-trapped during a second exposure to the same concentration of NTG in the presence of DETC. 5. Cytochrome P450 purified from rabbit liver enhanced NO formation in a NADPH-dependent fashion from NTG, but not from the other nitrates, as assessed by activation of purified soluble guanylyl cyclase. 6. We conclude that the vessel selective action of different organic nitrates in vivo reflects differences in vascular NO formation. Thus, efficient preload reduction by classical organic nitrates can be accounted for by higher NO formation in venous capacitance as compared to arterial conductance and resistance vessels. In contrast, NO is released from cysteine-containing nitrates (SPMs) to a similar extent in arteries and veins, presumably independently of an organic nitrate-specific biotransformation. Limited tissue bioavailability of NTG and ISDN might account for low NO formation in the aorta, while true differences in biotransformation seem to account for differences in NO formation in the other vascular tissues.

Animals↗
PubMed1997

Pericolic mesenteric lymph nodes: an aid in distinguishing diverticulitis from cancer of the colon.

OBJECTIVE: This study was done to determine if the detection of pericolic lymph nodes on CT scans could be used to differentiate cancer of the colon from diverticulitis. MATERIALS AND METHODS: We retrospectively evaluated 58 CT scans from 57 patients with proven diverticulitis or cancer of the colon. The CT scans were evaluated by five board-certified radiologists who were unaware of the proven diagnosis. Consensus opinions regarding the presence and size of pericolic lymph nodes were recorded. These data were correlated with the proven diagnoses to determine the correlation between the observed findings and the type of colonic abnormality. Fisher's exact test was used to determine statistical significance. RESULTS: Lymph nodes were seen in 22 (71%) of 31 cases of colonic cancer and in four (15%) of 27 cases of diverticulitis. The lymph nodes were 0.5-2.5 cm in short-axis diameter. We saw no difference in node size for patients with colonic cancer versus patients with diverticulitis. The nodes were most commonly located along the blood vessels in the mesenteric fat. Statistical analysis showed a significant difference (p < .001) in the frequency but not in the size of nodes between the two groups of patients. The detection of nodes resulted in a diagnostic sensitivity and specificity for colonic cancer of 71% and 85%, respectively. CONCLUSION: Pericolic lymph nodes are seen much more frequently in patients with colonic cancer than in patients with diverticulitis. The detection of pericolic lymph nodes in patients suspected of having diverticulitis should raise the suspicion of underlying colonic cancer that should, in turn, prompt additional evaluation.

Colonic Neoplasms↗
PubMed1991

Chronic nerve growth factor treatment of normotensive rats.

The objectives of this study were to examine the effects of chronic nerve growth factor (NGF) administration on vascular innervation and blood pressure in neonatal rats. Newborn Wistar-Kyoto (WKY) rats bred from normotensive parents were chronically treated with NGF for 8 weeks. Littermate controls received saline. Sympathetic ganglia of treated animals were greatly enlarged and in the superior cervical ganglion neuronal numbers were increased 200% and nuclear areas by 46%. The catecholamine contents of several sympathetically innervated tissues were determined biochemically and found to be significantly elevated in mesenteric arteries, aorta, ileum, adrenal and salivary glands from treated compared to control animals. The catecholamine concentrations were similar to, or exceeded those of the spontaneously hypertensive rat. Histochemically, an aberrant nerve supply was evident occupying a greater volume of the adventitia of the caudal artery and mesenteric arteries. In addition, nerve fibres could be seen penetrating the vessel wall to emerge within the lumen of mesenteric blood vessels. Analysis of the smooth muscle wall of the caudal artery revealed that a small but significantly hyperplastic response had been induced. Systolic blood pressures of NGF-treated and control animals were taken at one week intervals from 5 to 8 weeks of age utilizing the tail cuff method. The blood pressure of treated animals were within the normotensive range. It is concluded that chronic NGF treatment leads to changes in vascular innervation and muscle thickness that are similar to those seen in hypertensive animals. Furthermore, the results suggest the elevated levels of NGF seen in peripheral tissues of the spontaneously hypertensive rat are likely to be responsible for the hyperinnervation and resulting hyperplastic responses within vascular tissues, but not exclusively responsible for the elevated blood pressure.

Animals↗
PubMed1988

Vascular angiotensin converting enzyme activity in spontaneously hypertensive rats and its inhibition with cilazapril.

Angiotensin converting enzyme (ACE) activity was examined in large arteries and veins of rats and found to be present in most of the arteries and to a lesser extent in the veins, except for the femoral vessels which showed higher ACE activity in the vein than in the artery. For the aorta and all its branches, ACE activity was higher in the aorta and its branches in spontaneously hypertensive rats (SHR) than in age-matched normotensive Wistar-Kyoto rats (WKY), with the exception of the hepatic, pulmonary and basilar arteries where the levels were similar for SHR and WKY. For the vena cava and brachial vein, ACE activity was also higher in SHR than WKY but for most other veins the activity was the same with the exception of the pulmonary vein where ACE activity was higher in WKY. The acute treatment of SHR with cilazapril, an ACE inhibitor (0.3 and 3 mg/kg orally, for 4h) decreased aortic blood pressure and ACE activity in arterial and venous mesenteric and renal vessels in a dose-dependent fashion. Cilazapril, at the threshold hypotensive dose, markedly decreased ACE activity in each pair of aortic segments, carotid, pulmonary, subclavian, brachial and femoral vessels to a degree which was equivalent to that caused by the high dose. The effect outlasted a fall in blood pressure 24 h later. This was associated with a marked decrease in plasma angiotensin II and III and accumulation of angiotensin 1 at 4 h. No increase in plasma bradykinin or kallidin levels was detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Acute symptomatic abdominal aortic aneurysm secondary to endovascular stent graft associated type II endoleak.

Endovascular abdominal aneurysm repair (EVAR) is popular because of its low invasiveness and feasibility for high-risk patients. Endoleak is common after EVAR and is characterized by blood flow within the aneurysm sac but outside the stent graft. Type II or collateral endoleak commonly results from retrograde filling of the aneurysm from collateral visceral vessels, lumbar, inferior mesenteric, accessory renal or sacral arteries. Collateral leaks are generally thought to be benign and over half of the early leaks will seal spontaneously. Sporadically, collateral endoleak could lead to aneurysm sac pressurization and place the patient at ongoing risk of rupture. Herein, we report an uncommon case of early post-stent graft placement symptomatic abdominal aortic aneurysm associated with type II endoleak.

Aged↗
PubMedDate not supplied

Autoradiographic localization of peripheral [3H]-hydergine binding sites.

The anatomical distribution of the ergot derivative [3H]-hydergine (co-dergocrine mesylate) was analyzed by the use of an in vitro autoradiographic technique on frozen sections of rat heart, mesenteric and renal arteries, adrenal gland and kidney. In the heart, [3H]-hydergine was bound by atria and by myocytes of ventricles. In the arterial wall, the drug was bound primarily by the adventitia, by the adventitia-media border and by the intimal layer. The density of adventitial and adventitial-medial binding sites has an inverse relation with the diameter of mesenteric or renal vessels. In the adrenal gland, [3H]-hydergine was bound primarily by the medulla and, in lesser amounts, by the zona glomerulosa. In the kidney, the drug was localized within the arterial tree as well as in cortical tubules and in medullary collecting tubules. The above findings suggest that [3H]-hydergine is bound by various structures involved in the regulation of cardiovascular homeostasis. Interaction with these sites probably accounts for the antihypertensive action of hydergine.

Adrenal Glands↗