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PubMed1989

[The hepatic hemodynamic response to intra-arterial infusion of vasoactive agents--Part 2. Blood flow measurements in rats with liver cancer].

The tissue blood flow (TBF) of primary liver cancer and normal live in 54 rats were measured following infusion of vasoactive agents into the celiac axis under continuous recording of blood pressure. Angiotensin II (AT) (1.0 micrograms/kg/min) and Prostaglandin F2 alpha (PGF) (1.0 micrograms/kg/min) were used. The former increased TBF of the tumor and blood pressure and the latter reduced TBF of the tumor with no remarkable change of the blood pressure, but both drugs made little or no influence on TBF of the normal liver. Dibutyryl cyclic AMP (DBcAMP) (2.0 mg/kg/hr) infusion increased TBF of the both tumor and normal liver with no significant change of blood pressure. PGF (1.0 micrograms/kg/min) infusion after preinfusion of DBcAMP did not cause the decrease of TBF of the tumor.

Angiotensin II↗
PubMed1999

Regulation of ET-1 biosynthesis in cerebral microvascular endothelial cells by vasoactive agents and PKC.

Endothelin-1 (ET-1) is the most potent vasoconstrictor agent known. ET-1 is elevated in the cerebrospinal fluid following hemorrhage and brain injury and can compromise cerebral microvascular homeostasis. The modulation of ET-1 production by cerebral microvascular endothelial cells and the mechanism by which such changes take place are very important in our understanding of the pathological roles of ET-1. In the present study, we investigated the effects of vasoconstrictor agents that can be released from hemolyzed blood, cAMP-dependent dilators, and the role of protein kinase C (PKC) in the regulation of ET-1 production by piglet cerebral microvascular endothelial cells in culture. ET-1 was measured by RIA. 1) Cerebral microvascular endothelial cells synthesize and release ET-1 into the media; 2) 5-hydroxytryptamine (5-HT), lysophosphatidic acid (LPA), thromboxane analog U-46619, fetal bovine serum (20%), and phorbol 12-myristate 13-acetate significantly increase ET-1 production; 3) basal and vasoconstrictor agent-induced increases in ET-1 production by endothelial cells may be mediated via PKC; 4) cAMP-dependent vasodilators attenuate the basal production of ET-1 by cerebral microvessels; and 5) pretreatment of endothelial cells with a higher concentration of LPA, U-46619, or 5-HT counterbalances the cAMP-dependent dilator agent-induced reduction in basal ET-1 production. Therefore, by-products of hemolyzed blood can stimulate the production of ET-1 by a PKC-mediated mechanism. cAMP-dependent dilators can attenuate the vasoconstrictor agent-induced elevation in ET-1 production. These results suggest that cerebral microvascular homeostasis could be compromised by effects of interactions among vasoactive agents released during conditions injurious to the brain and they may further the understanding of potential contributions of hemolyzed blood clots to subarachnoid hemorrhage-induced vasospasm.

Animals↗
PubMed1982

Effect of an increased cardiac output on vascular responses to vasoactive agents in two-kidney, one-clip Goldblatt hypertension.

The effect of the increased cardiac output of two-kidney, one-clip Goldblatt hypertension (2-KGH) on the altered vascular responses to vasoactive agents was examined in the conscious, chronically instrumented dog. The early stage of 2-KGH is characterized by an increased arterial pressure, an increased aortic flow, a decreased total peripheral resistance, and enhanced responses to angiotensin II and serotonin. As the aortic flow increases the responses to norepinephrine are enhanced, and the dilator responses to acetyl-choline and nitroglycerin are depressed. Aortic flow then returns to control values and the increased arterial pressure is maintained by an increase in peripheral resistance. When the increased aortic flow is prevented by occluding the vena cava to maintain flow at control values, the vascular responses to each of the agonists do not differ from that obtained when the aortic flow is elevated. Moreover, the temporal development and magnitude of the elevation in arterial pressure resulting from the increased vascular resistance is similar in dogs with an increased and normal aortic flows. The results suggest that increased aortic flow is not essential for the increased vascular resistance or the vascular changes in the canine model of 2-KGH.

Acetylcholine↗
PubMed1992

Vasoactive agents affect growth and protein synthesis of cultured rat mesangial cells.

Mesangial cell (MC) proliferation and extracellular matrix (ECM) formation are hallmarks of chronic glomerular disease. The present in vitro study examined the effects of the vasoactive agents angiotensin II (Ang II), arginine vasopressin (AVP), and serotonin (5-HT) on growth and protein biosynthesis of cultured rat MCs after 72 hours of incubation. AVP and 5-HT (10(-6) M) significantly increased DNA synthesis and growth of quiescent subconfluent MCs to levels of 25 and 45%, respectively, of the optimal stimulatory effect of 10% fetal calf serum (FCS) (both P less than 0.001). The mitogenic effect of Ang II was 10% of the 10% FCS effect (P less than 0.01). ECM production was studied by ELISA assay for fibronectin (FN) secreted into the culture medium (SeFN) and cell-associated FN, that is, intra- and pericellular FN (CaFN). In all incubations, highly significant negative linear relationships were found between the numbers of MCs per well and quantities of both SeFN and CaFN after normalization of the data by logarithmic transformation (SeFN: r values greater than -0.9705; CaFN: r greater than -0.9620; P less than 0.001). Thus, increasing cell densities progressively suppressed ECM formation by MCs. The ECM production was found to be independent of growth activity. AVP significantly increased SeFN (P less than 0.05) and decreased CaFN (P less than 0.001) in subconfluent cultures; Ang II and 5-HT had no effect. Metabolic labeling with 35S-methionine (18 hr, 200 microCi/ml medium) and 2-D electrophoresis of MC lysates resulted in resolution of greater than 500 different radiolabeled intracellular proteins in molecular weight from 110 to 20 Kd over an isoelectric interval of 5.0 to 7.0.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1982

Withdrawal of magnesium enhances coronary arterial spasms produced by vasoactive agents.

1 The influence of external magnesium ions ([Mg2+]o) on the sensitivity (i.e. EC50) and contractility (maximum response) of isolated large and small coronary arteries of the dog, obtained from different regions of the myocardium, to vasoactive agents was studied. 2 Removal of [Mg2+]o from the physiological salt solution enhanced, while elevation in [Mg2+]o to 4.8 mM, lowered the contractile sensitivity to three different agents, 5-hydroxytryptamine (5-HT), angiotensin II and KCl. 3 Contractility, of both large and small coronary arteries, to 5-HT and angiotensin II was potentiated and depressed, respectively, by withdrawal and elevation of [Mg2+]o; maximum responses to KCl were not altered by 0 or 4.8 mM [Mg2+]o. 4 Cumulative concentration-contractile effect curves to CaCl2 were shifted leftward on removal of [Mg2+]o; elevation of [Mg2+]o to 4.8 mM shifted the CaCl2 concentration-effect curves to the right. Maximal contractile responses to CaCl2 were enhanced by removal of, and reduced by elevation of, [Mg2+]o. 5 The calcium channel blocking agent, verapamil (10(-6)M), inhibited completely contractile responses to KCl; contractile responses elicited by angiotensin II and 5-HT were attenuated by verapamil. 6 A variety of pharmacological antagonists (phentolamine, propranolol, methysergide, atropine, diphenhydramine), as well as use of a prostaglandin cyclo-oxygenase inhibitor, did not modify the altered contractile responses evoked by angiotensin II or KCl in different concentrations of Mg2+. 7 These results suggest: (1) [Mg2+]o may exert considerably greater influence on receptor-operated rather than membrane-potential sensitive channels involved in Ca2+ transport in coronary arterial smooth muscle; (2) Mg2+ interferes with the affinity (binding) of certain agonists (5-HT and angiotensin II) for their respective receptors in coronary vascular muscle; and (3) a functional pool of Ca2+ which is resistant to Ca2+-depletion, but accessible to activation by 5-HT and angiotensin II is present in canine coronary arterial smooth muscle.

Angiotensin Amide↗
PubMed1982

Oxygen transfer, gill resistance and structural changes in rainbow trout (Salmo gairdneri, Richardson) gills perfused with vasoactive agents.

1. Gill resistance (Rg) and oxygen transfer (To2) were measured in perfused rainbow trout gills. After perfusion the gills were analysed morphometrically. 2. Rg increased with 40% and To2 decreased with 91% during 60 min perfusion without vasoactive substances in the perfusion Ringer. 3. In presence of 10 micro M adrenaline both Rg and To2 remained stable at their starting levels throughout the experimental period (60 min). 4. With 0.2 micro M acetylcholine and 10 micro M adrenaline in Ringer Rg increased nearby to the same extent as in perfusions without vasoactive agents, while To2 was not significantly affected. 1 micro M acetylcholine increased Rg with 76% and decreased To2 with 51%. 5. The changes in Rg and To2 could be explained by structural changes in the secondary lamellae.

Acetylcholine↗
PubMed2005

Clinical and duplex US assessment of effects of sildenafil on cavernosal arteries of the penis: comparison with intracavernosal injection of vasoactive agents--initial experience.

PURPOSE: To prospectively evaluate the clinical response and hemodynamic changes in cavernosal arteries after oral administration of sildenafil without and with audiovisual sexual stimulation and to compare those responses with responses from intracavernosal injections of vasoactive agents. MATERIALS AND METHODS: Institutional review board approval and written informed consent were obtained. Thirteen consecutive patients (age range, 22-77 years; mean, 60.4 years) with erectile dysfunction were evaluated with clinical assessment and cavernosal duplex ultrasonography (US). The patients were examined at two sessions 3 weeks apart. First, each patient received 100 mg of sildenafil citrate orally and was examined 60 minutes later without any sexual stimulation. Each patient then underwent repeat clinical and duplex US assessment after audiovisual sexual stimulation. Three weeks later, the patients underwent identical clinical evaluation and duplex US after intracavernosal injection of a commercially available combination of papaverine, prostaglandin E1, and phentolamine. Clinical and duplex US data (ie, peak systolic velocity [PSV]) were examined by using the Wilcoxon signed rank test for matched pairs. RESULTS: At rest, the overall mean cavernosal artery PSV was 1.08 cm/sec and remained unchanged after intake of sildenafil without any audiovisual stimulation, with no clinical evidence of erection. With the addition of audiovisual sexual stimulation, eight (62%) of 13 patients had penile congestion or erection, and six (46%) had a PSV greater than 25 cm/sec. With intracavernosal injection of the combination of three drugs, all 13 patients achieved congestion or erection, and 10 (77%) had a PSV greater than 25 cm/sec. Both clinical and duplex US responses to intracavernosal injection were significantly greater than they were to sildenafil with audiovisual sexual stimulation (P = .04 and .003, respectively). CONCLUSION: Oral sildenafil with audiovisual sexual stimulation led to a significant clinical response and increment in blood flow in the cavernosal arteries. However, more patients responded to intracavernosal injection of the combination of three drugs than to sildenafil, and the clinical response was significantly better.

Administration, Oral↗
PubMed2006

Histamine, a vasoactive agent with vascular disrupting potential, improves tumour response by enhancing local drug delivery.

Tumour necrosis factor (TNF)-based isolated limb perfusion (ILP) is an approved and registered treatment for sarcomas confined to the limbs in Europe since 1998, with limb salvage indexes of 76%. TNF improves drug distribution in solid tumours and secondarily destroys the tumour-associated vasculature (TAV). Here we explore the synergistic antitumour effect of another vasoactive agent, histamine (Hi), in doxorubicin (DXR)-based ILP and evaluate its antivascular effects on TAV. We used our well-established rat ILP model for in vivo studies looking at tumour response, drug distribution and effects on tumour vessels. In vitro studies explored drug interactions at cellular level on tumour cells (BN-175) and Human umbilical vein endothelial cells (HUVEC). There was a 17% partial response and a 50% arrest in tumour growth when Hi was combined to DXR, without important side effects, against 100% progressive disease with DXR alone and 29% arrest in tumour growth for Hi alone. Histology documented an increased DXR leakage in tumour tissue combined to a destruction of the TAV, when Hi was added to the ILP. In vitro no synergy between the drugs was observed. In conclusion, Hi is a vasoactive drug, targeting primarily the TAV and synergises with different chemotherapeutic agents.

Animals↗
PubMed2002

Changes in the Doppler waveform of the ovine femoral artery following infusion of vasoactive agents: a preliminary study.

The aim of this study was to investigate whether femoral artery pulsatility index (PI) can be used as an indicator of vasomotor tone in the digit of an ungulate species by measuring the change in PI induced by infusion of vasoactive agents in halothane-anaesthetised sheep. Intra-arterial infusion of the vasoconstrictor phenylephrine (9 microg min(-1)) tended to increase waveform PI (3.89-6.24, n=4, P=0.100). Infusion of a low dose (3 microg min(-1)) of the vasodilator sodium nitroprusside did not alter femoral artery PI, however infusion of a higher dose (30 microg min(-1)) tended to increase PI (5.39-6.70, n=5, P=0.059). During these studies heart rate, mean ABP and p(a)CO(2) did not change significantly. The tendency for PI to increase in response to vasodilation was unexpected and the mechanism involved is unclear. It appears that femoral artery PI cannot be used to predict vasomotor tone in the digit of the anaesthetised sheep.

Anesthetics, Inhalation↗
PubMed1990

Enhancement of chemotherapy and nitroimidazole-induced chemopotentiation by the vasoactive agent hydralazine.

Nitroimidazoles have been shown to be potent sensitisers of certain clinically active chemotherapeutic agents. This process of chemopotentiation has been shown to be hypoxia-mediated. The present studies evaluated whether increasing the level of hypoxia in the tumour tissue, by treatment with the vasoactive agent hydralazine, could modify the chemosensitising ability of nitroheterocyclics. Administering either misonidazole or RSU 1164 before, or hydralazine after, the chemotherapeutic agents melphalan, cyclophosphamide or the nitrosourea CCNU, increased the extent of cell kill in both the KHT sarcoma and RIF-1 tumour. However, even greater enhancements could be achieved when hydralazine was used in treatment protocols in which a nitroimidazole was combined with chemotherapy. For example, a 5.0 mg kg-1 dose of hydralazine given 30 min after melphalan, or a 2.5 mmol kg-1 dose of misonidazole administered 30 min before melphalan, increased, compared to melphalan alone, the resultant tumour cell kill by factors of approximately 1.9 and approximately 1.3, respectively. By comparison, when hydralazine was given after the melphalan plus misonidazole combination, treatment efficacy was enhanced approximately 3-fold compared to melphalan alone. Yet in contrast to the results of the tumour response studies, the inclusion of hydralazine did not increase the bone marrow toxicity associated with the chemotherapeutic agent when used alone or in conjunction with a nitroimidazole. The results, therefore, imply that the addition of hydralazine to the chemotherapy, or chemotherapy-sensitiser protocol, led to a therapeutic advantage.

Animals↗
PubMed2001

A vasoactive agent enhances the effect of ATP on cochlear blood flow.

Adenosine 5'-triphosphate (ATP) has a dual effect on cochlear blood flow (CBF). It induces on initial, transient decrease, which is followed by a long-lasting increase in CBF. Dilazep dihydrochloride (DZ) is a unique vasoactive agent, which increases CBF as well as decreases systemic blood pressure (BP). This agent is thought to keep the concentration of extracellular adenosine higher than normal by preventing the absorption of adenosine into the intracellular space. Thus, it may potentiate the effect of ATP on CBF. In this study, the effects are reported of ATP on CBF in the presence of DZ as measured with a laser Doppler flowmeter in the guinea pig cochlea. In the presence of DZ, the effect of ATP on CBF was amplified and prolonged. Specifically, the mean value of CBF initially decreased to 30.0% of the baseline, determined prior to administration of any agent, and increased gradually up to 287.8% of the baseline. This pharmaceutical effect of DZ might involve a longer activation of both P2x- and P2y-purinoceptors.

Adenosine Triphosphate↗
PubMed2004

Serum vasoactive agents in rats poisoned with cadmium.

OBJECTIVES: Mechanisms of the vascular effect of cadmium vary and involve nervous, hormone and intracellular signaling pathways. However, it is still not clear if mechanisms of the vascular effect of cadmium (Cd) include changes in the synthesis or release of vasoactive agents. The aim of this study was to evaluate the impact of subchronic Cd poisoning on blood nitric oxide or endothelin in blood and to relate it to the redox system activity in vessel walls and to blood Cd concentration. MATERIALS AND METHODS: The study was performed on male Buffalo rats which were given cadmium in drinking water, 50 or 200 ppm, for 12 weeks. RESULTS: The study showed different dose-dependent changes in toxicological and biochemical status. Mean serum nitric oxide concentration (measured using R&D Systems) was lower in rats poisoned with cadmium compared with the control group (57.7 +/- 7.6 vs. control 65.0 +/- 4.9 micromol/l, p < 0.05), whereas the plasma endothelin-1 level (measured using enzymoimmunoassay) and serum prostaglandin PGF2alpha concentration (determined using R&D System) were similar in all animals. The lipid peroxides concentration (measured colorimetrically) was higher in the group treated with cadmium in a dose of 50 ppm than in controls (5.2 +/- 3.0 vs. controls 1.4 +/- 0.4 nmol/ml, p < 0.001) and gluthatione concentration was decreased in the group treated with cadmium in a dose of 200 ppm as compared with the control group, (1.3 +/- 1.2 vs. control 2.5 +/- 0.9, micromol/l p < 0.05). CONCLUSIONS: It is concluded, that cadmium induces oxidative stress in both doses, however, the activity of defending mechanisms depends on Cd dose. Oxidative stress can be responsible for decreased nitric oxide concentration in serum. We suppose that the mechanisms of the vascular effect of cadmium vary and are dose-dependent. Cd used in a dose of 50 ppm for three months induces more severe functional vascular disturbances than its dose of 200 ppm.

Analysis of Variance↗
PubMed1986

Vasoactive agents affect mesangial cell adhesion.

The formation and maintenance of stress fibers in cultured mesangial cells is associated with myosin light chain phosphorylation [Kreisberg et al. Am. J. Physiol. 249 (Renal Fluid Electrolyte Physiol. 18): F227-F235, 1985], a biochemical indicator for activation of actin-myosin interactions. Agents that elevate intracellular levels of adenosine 3',5'-cyclic monophosphate (cAMP) (e.g., isoproterenol) fragment stress fibers and cause myosin light chain dephosphorylation, whereas the addition of contractile agents such as arginine vasopressin (AVP) and prostaglandin E2 (PGE2) reverses these changes. Because stress fiber development in cultured cells is correlated with tight cell to substrate adhesion, we wanted to examine whether vasoactive agents have an effect on mesangial cell adhesion. Both isoproterenol and dibutyryl cAMP (DBcAMP) reduced mesangial cell adherence as measured by a trypsin assay (% detached cells: control 11 +/- 2.4%; isoproterenol plus isobutylmethylxanthine (IBMX) = 48.3 +/- 7.4%; DBcAMP = 29.3 +/- 3.7%; DBcAMP-IBMX = 73 +/- 4.4%). The areas of focal (adhesive) contacts between the cell and substratum as observed by interference-reflexion microscopy were also reduced, being replaced by areas of greater separation (% of the surface in contact with the substratum: control = 7.4 +/- 0.8%; isoproterenol-IBMX = 2.9 +/- 1.1%). Addition of PGE2 or AVP to the incubation medium containing the cAMP-elevating agents prevented the above changes. PGE2 or AVP alone increased mesangial cell adhesion (% detached cells: control 11 +/- 2.4%; PGE2 = 6.8 +/- 0.5%; AVP = 5.1 +/- 1.2%).(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

Synergism between prostanoids and other vasoactive agents.

BACKGROUND: Prostaglandin E2 is usually considered to be a vasodilator, but some vascular beds respond with weak vasoconstriction mediated by prostanoid EP3-receptors. We have used the guinea pig isolated thoracic aorta to examine the nature of the synergism between the EP3 agonist sulprostone and other vasoactive agents. METHODS: Muscle tension was recorded from endothelium-denuded rings of aorta suspended in conventional organ baths. Indomethacin and the TP-receptor antagonist GR 32191 were usually present. RESULTS: Sulprostone (0.1-300 nM) showed two profiles: low-responder preparations (maximum response = 15-35% of 100 nM U-46619 response) were insensitive to the L-type Ca2+ blocker nifedipine, whereas high-responders (maximum = 35-70%) showed a nifedipine-sensitive component at higher sulprostone concentrations only. Charybdotoxin (CTX), a blocker of large-conductance Ca2+-activated K+ channels (BKCa), slightly enhanced threshold sulprostone responses and markedly enhanced larger responses; the enhancements were abolished by nifedipine. In contrast, threshold sulprostone responses were dramatically enhanced in the presence of established small contractions to phenylephrine (alpha1-adrenoceptor agonist), U-46619 (TP agonist), cyclopiazonic acid (sarcoplasmic Ca2+ pump inhibitor), and 4-aminopyridine (4-AP, Kv channel blocker). Nifedipine had no effect on enhancements of threshold sulprostone responses, and partially inhibited the enhancements of larger responses. CONCLUSIONS: BKCa channel activation appears to increase progressively as sulprostone-induced contraction increases. CTX removes this "BKCa brake," thereby providing an "L-type channel" Ca2+ flux to prime the EP3-receptor-driven Ca2+-sensitization mechanism (via Rhokinase activation, unpublished observations). In contrast, the other agents, including 4-AP, direct a non-L-type channel source of Ca2+ to the calmodulin-myosin light chain arm.

Animals↗
PubMed1988

Acute effects of noradrenalin related vasoactive agents on the ototoxicity of aspirin: an experimental study in the guinea pig.

Aspirin is known to be ototoxic when administered at high doses. Its mode of action is unknown but an alteration of the vascular function has been suspected. To further document this hypothesis, acute effects of some vasoactive agents on the ototoxicity of aspirin were tested in experiments on the guinea pig using sensori-neural electrophysiological responses and morphometry of the vessels of the stria and the spiral lamina. Electrophysiological measures showed no modification of sensory responses but neural responses revealed clear changes after administration of noradrenalin related agents, limited modifications after a drug acting partly as a serotonin antagonist, and no change after a dopaminergic agent. Morphometric studies showed no modification of the strial but some effect on the spiral vessels. The results are compatible with the hypothesis of a vascular involvement in the ototoxicity of aspirin and they point toward an interaction with the noradrenergic sympathetic cochlear system in the spiral lamina.

Animals↗
PubMed1991

Responses of subcultured rat aortic smooth muscle myocytes to vasoactive agents and KCl-induced depolarization.

We have developed a culture system in which a single-mass primary culture can be used for as long as 6 wk as a source of subcultured smooth muscle myocytes for the study of the changes of their shape upon addition of vasoactive agents (angiotensin, vasopressin, norepinephrine, and serotonin) and KCl depolarization. Responses of subcultivated myocytes were shown to be reproducible with time in primary culture before subculture and consistent with responses of thoracic aorta to the same agents. Effect of KCl depolarization could be blocked with calcium antagonist PN 200-110. Consistently, the presence of calcium L-channels was shown using whole cell patch-clamp recordings. A comparative study of the responses of myocytes derived from two different segments of the thoracic aorta showed that these cells displayed responses with different maximal amplitudes and the same potencies according to their topological origin in the vessel.

Angiotensin II↗
PubMedDate not supplied

Constriction of canine prenodal lymphatic vessels following the intra-arterial injection of vasoactive agents and hemorrhage.

In the forelimbs of anesthetized dogs, perfused at constant arterial inflow, we measured the pressure in a prenodal lymphatic vessel before and following arterial hemorrhage to a mean systemic arterial pressure of approximately 55 mmHg. We also made bolus intra-arterial injections of 1 microgram epinephrine and arginine vasopressin or 20 micrograms dopamine, prostaglandin F2 alpha and tyramine. Hemorrhage and all vasoactive substances significantly increased forelimb perfusion pressure and skin small artery pressure. Skin small vein pressure was significantly decreased by hemorrhage or injection of epinephrine, dopamine or tyramine, but was not significantly altered by arginine vasopressin or prostaglandin F2 alpha. Mean systemic arterial pressure was decreased by hemorrhage, increased by arginine vasopressin, tyramine and prostaglandin F2 alpha but remained unchanged following the injection of either epinephrine or dopamine. Lymphatic pressure was significantly increased following hemorrhage or the injection of all vasoactive agents. The increase seen with tyramine was small but consistent and thus statistically significant. These data indicate that the prenodal lymphatic vessels of the canine forelimb actively constrict in response to the neural and/or hormonal consequences of arterial hemorrhage or the introduction of exogenous vasoactive substances into the arterial blood supply to the forelimb. The results of the current study support the possibility that lymphatic function, through activation of lymphatic smooth muscle, is subject to neural and/or hormonal regulation in certain physiological and/or pathophysiological states.

Animals↗