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At least 73 records · Page 4Linked to original sources
PubMed2004

Advanced glycation endproduct crosslinking in the cardiovascular system: potential therapeutic target for cardiovascular disease.

Advanced glycation endproducts (AGEs) are formed by a reaction between reducing sugars and biological amines. Because of their marked stability, glycated proteins accumulate slowly over a person's lifespan, and can contribute to age-associated structural and physiological changes in the cardiovascular system such as increased vascular and myocardial stiffness, endothelial dysfunction, altered vascular injury responses and atherosclerotic plaque formation. The mechanisms by which AGEs affect the cardiovascular system include collagen crosslinking, alteration of low-density lipoprotein molecules and impairment of cellular nitric oxide signalling through their interaction with AGE receptors (RAGEs). Thus, the accumulation of AGEs may help to explain the increased cardiac risk associated with aging as well as diabetes mellitus and hypertension, two conditions that accelerate and enhance AGE formation. A variety of new pharmacological approaches are being developed to reduce the pathophysiological impact of AGEs. These agents can prevent AGE and AGE crosslink formation, break pre-existing AGE crosslinks, and block the interaction between AGEs and RAGEs. Such agents have been shown to reduce vascular and myocardial stiffness, inhibit atherosclerotic plaque formation and improve endothelial function in animal models. Improvement in vascular compliance has also been demonstrated with AGE crosslink breakers in clinical trials. These studies offer promise to reduce the cardiac risk associated with isolated systolic hypertension, diastolic dysfunction and diabetes.

Cardiovascular Diseases↗
PubMed1994

Neuropeptide Y and regulation of the cardiovascular system.

CONTROL OF CARDIOVASCULAR SYSTEM: Neuropeptide Y has three major activities which are important in the modulation of blood pressure homeostasis. When released from sympathetic neurons innervating the cardiovascular system, this peptide causes direct long-lasting vasoconstriction, inhibits the release of noradrenaline and other neurotransmitters and potentiates the action of noradrenaline and other pressor agents. RECEPTOR SUBTYPE DIVERSITY: At least two major subtypes of neuropeptide Y receptor have been defined by pharmacological criteria, and the major subtype involved in the control of blood pressure (Y1) has been isolated by molecular cloning. Analysis of the cloned DNA sequence has confirmed that the receptor is a member of the G protein-coupled receptor superfamily and when expressed in various cell lines can couple to both the inhibition of adenylate cyclase and the elevation of intracellular calcium. NEUROPEPTIDE Y ANTAGONISTS: A specific neuropeptide Y antagonist has been developed which significantly lowers the dose-dependent neuropeptide Y-induced pressor response in normal rats. The inhibition is specific for the peptide and also selective for the postsynaptic Y1 receptor-mediated vasoconstrictor activity. Administration of this specific and selective inhibitor significantly reduces resting arterial blood pressure, which remains depressed for up to 4 h in normal and spontaneously hypertensive rats. CONCLUSIONS: Inhibition of endogenous neuropeptide Y activity demonstrates that this peptide makes a significant contribution to the control of blood pressure and indicates the therapeutic potential of neuropeptide Y inhibitors as a new class of antihypertensive agent. The molecular cloning of the neuropeptide Y receptor subtype responsible for both the direct vasoconstrictor activity of the peptide and the potentiation of the action of other pressor agents represents an important advance in our understanding of the molecular basis of neuropeptide Y action and will help in the development of selective neuropeptide Y antagonists.

Amino Acid Sequence↗
PubMed2006

Neural crest contribution to the cardiovascular system.

Normal cardiovascular development requires complex remodeling of the outflow tract and pharyngeal arch arteries to create the separate pulmonic and systemic circulations. During remodeling, the outflow tract is septated to form the ascending aorta and the pulmonary trunk. The initially symmetrical pharyngeal arch arteries are remodeled to form the aortic arch, subclavian and carotid arteries. Remodeling is mediated by a population of neural crest cells arising between the mid-otic placode and somite four called the cardiac neural crest. Cardiac neural crest cells form smooth muscle and pericytes in the great arteries, and the neurons of cardiac innervation. In addition to the physical contribution of smooth muscle to the cardiovascular system, cardiac neural crest cells also provide signals required for the maintenance and differentiation of the other cell layers in the pharyngeal apparatus. Reciprocal signaling between the cardiac neural crest cells and cardiogenic mesoderm of the secondary heart field is required for elaboration of the conotruncus and disruption in this signaling results in primary myocardial dysfunction. Cardiovascular defects attributed to the cardiac neural crest cells may reflect either cell autonomous defects in the neural crest or defects in signaling between the neural crest and adjacent cell layers.

Animals↗
PubMed1996

[The participation of nitric oxide in the functions of the central nervous system and the cardiovascular system].

Nitric oxide (NO) exerts its vasodilatator effect in smooth muscle by activation of guanylyl cyclase. This in turn leads to decreases in intracellular calcium and dephosphorylation of myosin light chains and relaxation. NO is synthesised from L-arginine by a family of enzymes called Nitric oxide synthase (NOS). In the vascular system two isoenzymes of NOS are largely expressed: the constitutive NOS and the inducible NOS. The constitutive NOS identified in the endothelium generates NO continuously providing the vasodilatator tone and modulating platelet function. NOS type 1 is expressed in preoptic and infundibular nucleus of hypothalamus. NO acts as presynaptic agonist of glutamatergic NMDA-receptor mediation in the motor nucleus of nervus vagus. NO decreases the frequency of the spontaneous discharges in the carotid bodies. NO is involved in the processes of synaptic plasticity in the hippocampus.

Animals↗
PubMed2003

Use of a telemetry system to examine recovery of the cardiovascular system after excitement induced by handling stress in a conscious cynomolgus monkey (Macaca fascicularis).

The aim of this study was to determine the time required for the cardiovascular system of a conscious cynomolgus monkey, in which a telemetry had been implanted, to recover from excitement induced by handling stress. With enforcement of guidelines regarding safety pharmacological studies, cardiovascular studies in primates have become more important. However, as macaque monkeys are promptly excited under experimental procedures, it is often difficult to evaluate the drug effects on the cardiovascular system. Therefore, we tested monkey chair restraint and intravenous injection of saline. After monkey chair restraint and intravenous injection, approximately 30 minutes were required for recovery of both heart rate and blood pressure to their pre-treatment level; however, ECG parameters such as PR, QRS interval, and QTc did not drastically change. Based on our current results and with sufficient consideration of autonomic nervous effects, accurate evaluation of drug effects on the cardiovascular system should now be possible.

Animals↗
PubMed1976

[Effects of fusaric acid and its derivative on the cardiovascular system].

The cardiovascular effects of fusaric acid, a dopamine-beta-hydroxylase (DBH) inhibitor and a hypotensive agent, and 5-(4'-chlorobutyl) picolinic acid, one of the most potent DBH inhibitors in fusaric acid derivatives, were investigated in anesthetized dogs. Fusaric acid (10-30 mg/kg) given intravenously caused immediately and dose-dependently a fall in blood pressure, an increase in heart rate, a stimulation of respiration, a marked increase in the rate of superior mesenteric arterial flow, and a decrease in the rate of femoral arterial flow. Fusaric acid (0.3-3 mg) given close-arterially caused a dose-dependent decrease in the sinus rate and in the developed tension in isolated blood-perfused sinoatrial node and papillary muscle preparations, respectively. For the superior mesenteric, renal, and femoral circulations which were perfused with blood, a close-arterial injection of fusaric acid (10-30 mg) increased in the rates of flow in a dose-dependent manner. 5-(4'-Chlorobutyl) picolinic acid showed similar responses as fusaric acid quantitatively or qualitatively. These results indicate that hypotension induced rapidly after intravenous administration of fusaric acid or 5-(4'-chlorobutyl) picolinic acid is not due to the enzyme inhibition, but rather to the direct depression of cardiac function and decrease in peripheral vascular resistance.

Animals↗
PubMed1984

[Pharmacological studies on new cephamycin, MT-141. (1) Its effect on central nervous system, respiration and cardiovascular system].

The results on pharmacological effects of MT-141 were as follows. MT-141 did not exert effect on central nervous system in mice and rabbits but potentiated the anesthetic effect of thiopental at doses above 800 mg/kg i.v. MT-141 slightly raised a level of blood pressure in dogs and also caused a slight increase in the blood flow and heart rate when intravenously given more than 400 mg/kg. This compound did not affect the spontaneous contraction of isolated guinea pig atria and the blood vessels in perfused rabbit ears. MT-141 did not significantly affect the spontaneous contraction and coronary flow in isolated hearts of guinea pig. The body temperature was raised slightly by an injection of more than 400 mg/kg of MT-141. These results suggest that MT-141 does not possess specific effect on central nervous system but at a high dose slightly affects the autonomic nervous system such as blood pressure, body temperature, heart rate and blood flow in experimental animals.

Animals↗
PubMed1992

Cardiovascular simulation using a multiple modeling method on a digital computer--simulation of interaction between the cardiovascular system and angiotensin II.

A cardiovascular system model that simulates interactive responses to drugs has been developed on a small digital computer. The overall model basically consists of three models. The first is a momentum transport model that represents relations between blood pressure and flow in the cardiovascular system. In this model, the cardiovascular system is divided into 14 components and modeled by using equivalent electrical circuits. The second is a mass transport model comprising 14 compartments corresponding to the respective components of the cardiovascular system. This model represents the distribution of the administered drug in the various cardiovascular components. The third is an interaction model that represents the relationships between the momentum and mass transport models. This model causes variations in the resistance and capacitance parameters of the momentum transport model as a function of the current drug concentrations in the appropriate compartments of the mass transport model. The capacitances representing the ventricles are varied in a time-dependent fashion to simulate the beat of the heart. Simulation is performed by using the Euler method to solve a system of 28 ordinary differential equations governing the momentum and mass transport models on a 32-bit microcomputer, a Macintosh II. The model was assessed by performing two demonstrations of the cardiovascular response to the vasopressor angiotensin II (AT II). They first examined the interaction between the cardiovascular system and AT II. The effect of AT II on the cardiovascular system was incorporated into the interaction model. Administration of AT II as a constant infusion (200 micrograms/hr) resulted in an elevation of mean arterial pressure from approximately 100 to 150 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗