arterial pressure

Captopril (SA333) is a potent and specific inhibitor of peptidyl-dipeptidase A. It blocks the conversion of angiotensin I to angiotensin II, a vasoconstrictor and important regulator of arterial blood pressure.

[Sar9,Met(O2)11]-Substance P acetate is a tachykinin NK1 receptor selective agonist. [Sar9,Met(O2)11]-Substance P acetate is a selective tachykinin NK1 receptor agonist.[Sar9,Met(O2)11]-Substance P acetate and septide (10-100 pmol per rat, i.c.v.) are equipotent in increasing mean arterial blood pressure (MAP) and heart rate (HR), yet they have dissimilar time-course. Both agonists increase dose-dependently face washing and sniffing while [Sar9,Met(O2)11]-Substance P acetate is the sole to produce grooming.

Benzoquinamide hydrochloride (3-carbamoyl-N,N-diethyl-1,3,4,6,7,11b-hexahydro-9,11-dimethoxy-2H-benzo[a]quinolizin-2-yl acetate hydrochloride) is an antiemetic agent and increases intra-arterial pressure due to the increased peripheral vascular resistance.

Propanidid (Sombrevin) is a gamma-aminobutyric acid type A receptor (GABAA) agonist and a fast-acting intravenous anesthetic that lowers arterial blood pressure.

Potent apelin (APJ) receptor agonist (Ki = 0.93 nM). Bioactive fragment of ELA-32. Activates Gαi1 pathway and β-arrestin-2 recruitment. Reduces arterial pressure in rat hearts. Active in vivo.

Auriculin A, a synthetic atrial natriuretic factor (ANF), exhibits hemodynamic properties by antagonizing renal vasoconstriction in dogs and affects arterial baroreflex regulation of heart rate, systemic blood pressure, and constant flow-perfused hind limb perfusion pressure in rabbits [1] [2].

Chlorthalidone impurity G is a potential impurity found in commercial preparations of chlorthalidone that has moderate antihypertensive effects. Chlorthalidone is a thiazide-like diuretic that inhibits the Na+/Cl- cotransporter in the distal convoluted tubule of the kidney, which prevents reabsorption of sodium and chloride leading to a reduction in plasma volume and cardiac output. It also inhibits carbonic anhydrase (CA), including the isoforms CAVB, VII, IX, XII, and XIII (Kis = 2.8-23 nM) and, to a lesser extent, CAI, CAII, IV, VA, and VI (Kis = 138-1,347 nM), which may mediate its sustained vasodilatory activity. Dietary administration of chlorthalidone (8 mg per animal per day) reduces arterial hypertension and prevents or reduces ventricular hypertrophy induced by deoxycorticosterone acetate (DOCA) in salt-hypertensive rats. Formulations containing chlorthalidone have been used alone or in combination with other antihypertensive agents to lower arterial blood pressure and as adjuvants to address edema caused by cardiac or renal disorders.

LPLRF-NH2, an RFamide peptide, exhibits an anorexigenic effect, elevates arterial blood pressure, and alters brainstem neuronal electrical activity [1] [2] [3].

Methyl diethyldithiocarbamate is an active metabolite of the aldehyde dehydrogenase inhibitor disulfiram .1It is produced by methylation of the disulfiram metabolite diethyldithiocarbamate in mouse liver microsomes.2Methyl diethyldithiocarbamate inhibits liver low Kmaldehyde dehydrogenase (ALDH) in rats (ID50= 15.5 mg/kg).1It decreases mean arterial pressure (MAP) and increases heart rate during ethanol challenge in rats when administered at a dose of 20.6 mg/kg. 1.Hart, B.W., Yourick, J.J., and Faiman, M.D.S-methyl-N,N-diethylthiolcarbamate: A disulfiram metabolite and potent rat liver mitochondrial low Km aldehyde dehydrogenase inhibitorAlcohol7(2)165-169(1990) 2.Gessner, T., and Jakubowski, M.Diethyldithiocarbamic acid methyl ester. A metabolite of disulfiramBiochem. Pharmacol.21(2)219-230(1972)

Urocortin II, a neuropeptide hormone within the corticotropin-releasing factor (CRF) family—which comprises mammalian CRF, urocortin I, urocortin III, frog sauvagine, and piscine urotensin I—displays 34, 43, and 37-40% sequence homology with rat and human CRF, human urocortin I, and human urocortin III, respectively. This compound enhances rabbit ventricular myocyte shortening and relaxation in both a time- and concentration-dependent manner. In vivo studies reveal that urocortin II lowers arterial blood pressure in both normotensive and spontaneously hypertensive rats through peripheral CRF2 receptor agonism, inducing dose-dependent tachycardia and hypotension at doses of 3 and 30 pmol/kg. Additionally, it mitigates the visceral pain response to colorectal distension at 10 and 20 μg/kg in conscious rats and delays gastric emptying in mice.

LDN-27219 is a potent hTGase inhibitor with IC50 of 0.6 uM.

Thrombin receptor agonist peptide (TRAP-14) is a 14-amino acid peptide agonist of the α-thrombin receptor. It induces aggregation of washed platelets as well as platelets in citrated and hirudin plasma. TRAP-14 (100 μM) increases the cytosolic calcium concentration in isolated guinea pig pulmonary smooth muscle cells 5-fold over baseline. It increases pulmonary arterial pressure in isolated guinea pig lung when used at a concentration of 1 μM, which is comparable to the effect induced by 10 nM α-thrombin. TRAP-14 also induces contraction of isolated rat aortic rings and increases endothelin-1 (ET-1) levels in a dose-dependent manner, an effect that is reversed by the ETA antagonist BQ-123 and the nitric oxide synthase (NOS) inhibitor L-NNA .

Quinapril-d5 is intended for use as an internal standard for the quantification of quinapril by GC- or LC-MS. Quinapril is a prodrug form of the angiotensin converting enzyme (ACE) inhibitor quinaprilat. In vivo, quinapril reduces mean arterial pressure in renal hypertensive and spontaneously hypertensive rats. It inhibits angiotensin I-induced pressor responses in normotensive rats and dogs. Quinapril prevents left ventricular heart failure in CHF 14.6 cardiomyopathic hamsters. Formulations containing quinapril have been used in the treatment of hypertension, heart failure, and diabetic nephropathy.

CDDO-dhTFEA, a synthetic oleanane triterpenoid, effectively activates Nrf2 while inhibiting the NF-κB pro-inflammatory transcription factor. It restores mean arterial pressure (MAP), elevates Nrf2 levels and the expression of related genes, attenuates NF-κB and transforming growth factor-β pathway activation, and mitigates glomerulosclerosis, interstitial fibrosis, and inflammation in rats with chronic kidney disease (CKD).

(Phenylac1,D-Tyr(Et)2,Lys6,Arg8,des-Gly9)-Vasopressin, a potent vasopressin V1 receptor (VP V1R) antagonist, significantly lowers mean arterial pressure (MAP) in rats [1].

Tempone is an aminooxyalkane that acts as a free radical scavenger and reacts with reactive oxygen species (ROS). Intravenous Tempone reduces mean arterial pressure in spontaneously hypertensive rats.

Chloracyzine can produce a decrease in myocardial oxygen consumption accompanied by a reduction in coronary blood flow preceded by transient coronary dilatation. It produced an insignificant increase in arterial pressure; heart rate increased slightly in

Moexiprilat, an active metabolite of the prodrug moexipril formed through side chain ester hydrolysis in vivo, functions as an angiotensin-converting enzyme (ACE; IC50 = 2.1 nM) inhibitor. At a concentration of 10 nM, it inhibits the proliferation of primary neonatal rat cardiac fibroblasts stimulated by estrone or angiotensin II. Furthermore, when given at a daily dosage of 50 mg/kg, moexiprilat reduces mean arterial blood pressure and elevates levels of atrial natriuretic peptide, an indicator of hypertension, in ovariectomized mice.

Proadrenomedullin N-terminal 12 peptide (PAMP-12), an endogenous fragment originating from the adrenal medulla and spanning amino acids 9-20 of human PAMP-20, plays a role in causing hypotension. It functions as an agonist for the MAS-related G protein-coupled receptor family member X2 (MRGPRX2), inhibiting forskolin-stimulated cAMP accumulation in CHO cells expressing human MRGPRX2 (EC50 = 57.2 nM) and selectively prompting calcium mobilization in these cells (EC50 = 41 nM), but not in cells expressing MRGPRX1, MRGPRX3, or MRGPRX4 at 1 µM. As an antagonist of nicotinic acetylcholine receptors (nAChRs), PAMP-12 obstructs carbachol-triggered catecholamine release and the influx of calcium and sodium (IC50s = 1.3, 0.39, and 0.87 µM, respectively) in primary bovine adrenal chromaffin cells, with no effect on histamine-induced responses (IC50s = >1 µM for all). Additionally, it decreases mean arterial blood pressure in normotensive rats at doses ranging from 10 to 50 nmol/kg.

2-Chloroadenosine-5'-O-diphosphate, a purine nucleotide adenosine 5'diphosphate (ADP) derivative, demonstrates multiple biological activities. It promotes aggregation and inhibits cyclic AMP (cAMP) production, triggered by prostaglandin E2 (PGE2), in a concentration-dependent manner within isolated human platelet-rich plasma. Additionally, this compound facilitates the relaxation of precontracted isolated guinea pig taenia coli strips (pD2 = 6.74) and reduces arterial blood pressure in rats. Moreover, 2-Chloroadenosine-5'-O-diphosphate significantly inhibits the ATPase activity of mortalin, a member of the heat shock protein 70 (Hsp70) family, with an apparent Ki of 45.05 µM for the human enzyme.

15-epiProstaglandin A1 (15-epiPGA1) is an R-stereoisomer of PGA1, belonging to the A-series prostaglandins derived from gorgonian soft corals. PGA1 is known for its effects on renal vasodilation, promoting sodium excretion through urine, and reducing arterial pressure in hypertensive individuals. However, the specific biological activities of 15-epiPGA1 have not yet been documented in published reports.

Arecaidine propargyl ester is an agonist of M2muscarinic acetylcholine receptors (mAChRs).1It selectively binds to M2over M1, M3, M4, and M5mAChRs in CHO cells expressing the human receptors (Kis = 0.0871, 1.23, 0.851, 0.977, and 0.933 μM, respectively). Arecaidine propargyl ester induces contractions in isolated guinea pig atrium (pD2= 8.67). It induces apoptosis and the production of reactive oxygen species (ROS) in U87 and U251 glioblastoma cells when used at a concentration of 100 μM.2Arecaidine propargyl ester decreases mean arterial blood pressure in normotensive cats (ED25= 1.9 nmol/kg).3It is toxic to house flies (Musca) when administered at a dose of 75 μg/fly.4 1.Scapecchi, S., Matucci, R., Bellucci, C., et al.Highly chiral muscarinic ligands: the discovery of (2S,2’R,3’S,5’R)-1-methyl-2-(2-methyl-1,3-oxathiolan-5-yl)pyrrolidine 3-sulfoxide methyl iodide, a potent, functionally selective, M2 partial agonistJ. Med. Chem.49(6)1925-1931(2006) 2.Di Bari, M., Tombolillo, B., Conte, C., et al.Cytotoxic and genotoxic effects mediated by M2 muscarinic receptor activation in human glioblastoma cellsNeurochem. Int.90261-270(2015) 3.Porsius, A.J., and Van Zwieten, P.A.Central action of some cholinergic drugs (arecaidine esters) and nicotine on blood pressure and heart rate of catsProg. Brain Res.47131-135(1977) 4.Honda, H., Tomizawa, M., and Casida, J.E.Insect muscarinic acetylcholine receptor: Pharmacological and toxicological profiles of antagonists and agonistsJ. Agric. Food Chem.55(6)2276-2281(2007)

Adrenomedullin (22-52) is a C-terminal fragment of adrenomedullin (1-52) . In vitro, adrenomedullin (22-52) reduces basal corticosterone production in a mixture of rat adrenocortical and adrenomedulllary cells. It also reverses increases in ACTH-stimulated corticosterone production induced by adrenomedullin (1-52). Adrenomedulin (22-52) (0.5 and 5 μg/kg/min) has no effect on basal regional cerebral blood flow but reverses increases in regional cerebral blood flow induced by rat adrenomedullin in rats. Unlike adrenomedullin (1-52), adrenomedullin (22-52) has no effect on mesenteric arterial perfusion pressure in cats.

Parathyroid hormone (PTH) (1-13) is an N-terminal fragment of PTH (1-34) . In vivo, PTH (1-13) (0.003-1 μmol/kg) increases mean arterial pressure (MAP) in anesthetized rats.

TRAP-6 peptide is a hexapeptide corresponding to residues 42-47 of protease-activated receptor 1 (PAR1). It acts as an agonist of PAR1, inducing platelet aggregation in human platelet-rich plasma ex vivo (EC50 = 0.8 μM). TRAP-6 (0.3 and 0.6 mg/kg) has a triphasic effect on mean arterial blood pressure (MAP) in anesthetized rats with a short decrease, an increase, and then a longer decrease in MAP following intravenous administration.

Adrenomedullin (13-52) is a truncated form of adrenomedullin (1-52) . It induces nitric oxide-dependent relaxation of and inhibits release of angiotensin II and endothelin-1 from isolated rat aorta. In vivo, adrenomedullin (13-52) decreases mean arterial pressure (MAP) in spontaneously and renal hypertensive rats in a dose-dependent manner. Adrenomedullin (13-52) (10-3,000 ng per animal) reverses increases in lobar arterial pressure induced by U-46619 in a dose-dependent manner in cats but has no effect on basal lobar arterial pressure or systemic arterial pressure. It also potentiates inflammatory edema and neutrophil accumulation in rats.

R 715, a bradykinin B1 receptor antagonist, inhibits contractions in isolated human umbilical cords that express bradykinin B1 receptors (pA2 = 8.49). When administered at doses of 200, 400, and 600 µg/kg, R 715 enhances latency to tail withdrawal in the tail-flick test for diabetic neuropathy mouse models induced by streptozotocin (STZ), signaling potential analgesic properties. Furthermore, at a 1 mg/kg per day dosage, it mitigates symptoms in a mouse model of experimental autoimmune encephalomyelitis (EAE) induced by MOG35-55 antigen peptide, such as reducing hind limb weakness and paralysis, improving gait symmetry, and decreasing spinal inflammation, neuron demyelination, and lesion monocyte invasion. Additionally, R 715 at 0.01 nmol/animal, administered intracerebroventricularly (i.c.v.), lowers mean arterial blood pressure and increases heart rate in spontaneously hypertensive rats, indicating cardiovascular effects.

Lithocholic acid 3-sulfate disodium (Sulfolithocholic acid disodium) acts as a RORgammat ligand and inhibits Th17 cell differentiation.Lithocholic acid 3-sulfate disodium is a sulfated product of lithocholic acid (LCA) and induces a decrease in arterial blood pressure. Lithocholic acid 3-sulfate disodium is a sulfated product of lithocholic acid (LCA) that induces cellular damage.

BMS 182874 is an orally effective and highly selective endothelin receptor ETA antagonist with an IC50 value of 0.150 μM for ETA and a Ki value of 0.055 μM for ETA.BMS 182874 is able to reduce arterial pressure in a rat hypertension model induced by Deoxycorticosterone acetate. BMS 182874 was able to reduce Deoxycorticosterone-induced arterial pressure in a rat model of hypertension and can be used to study cardiovascular disease.

A-192621 is a potent, nonpeptide, orally active and selective endothelin B (ETB) receptor antagonist with an IC50 of 4.5 nM and a Ki of 8.8 nM. A-192621 promotes apoptosis in PASMCs and it also causes elevation of arterial blood pressure and an elevation

Elabela(19-32) TFA, an effective fragment of ELABELA (ELA), selectively engages with the apelin receptor (APJ). This compound initiates G αi1 and β-arrestin-2 signaling, demonstrating EC50 values of 8.6 nM and 166 nM, respectively. It facilitates receptor internalization, lowers arterial pressure, and has a positive inotropic impact on cardiac function [1].

Ciprokiren is a renin inhibitor discovered by Roche. Ciprokinen inhibited human renin in a buffer and human plasma with an IC50 of 0.07 and 0.65 nmol/L, respectively. In animal models, acute and chronic administration of ciprokinen lead to a reduction in arterial blood pressure. Development of ciprokinen was discontinued at a preclinical stage.

[Sar9,Met(O2)11]-Substance P TFA is a selective tachykinin NK1 receptor agonist.[Sar9,Met(O2)11]-Substance P and septide (10-100 pmol per rat, i.c.v.) are equipotent in increasing mean arterial blood pressure (MAP) and heart rate (HR), yet they have dissi

Gepefrine, an orally active pressor and sympathomimetic agent, enhances the initial orthostatic regulation of arterial pressure.

Quinapril hydrochloride (PD-109452-2) is an angiotensin-converting enzyme (ACE) inhibitor used in the therapy of hypertension and congestive heart failure. Quinapril hydrochloride is associated with a low rate of transient serum aminotransferase elevations, but has yet to be linked to instances of acute liver injury.