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PHPY 304- Into CV Pharmacology

Terms in this set (36)

Neuro-Sympathetic Mediators
1) Methaoxamine (a1 activation)
2)Norepinephrine (a1, a2, B1)
3) Epinephrine (a1, a2, B1, B2)
4) Isoproterenol (B1, B2, B3)
Neuro-Parasympatherics Mediators
1) Acetylcholine; decreases HR
Endocrine System Mediators
1)Angiotensin II
2) Aldosterone
3) Vasopressin (ADH)
4) ANP
Paracrine System Mediators; Endothelial
1) Nitric Oxide (NO)
2) Endothelia-1 (ET-1)
Local Control Mediators
1)Antacids (myogenic tone)
2) Lactic acid, pH (metabolic factors)
Remote Control Systems (Extrinsic)
- Regulate BP and Blood Vol.
- Nervous System Innervations (Major key)
- Blood vessels are primarily innervated by the SNS.
Baroreceptors
Mechanoreceptors located in the carotid sinus and in the aortic arch. Their function is to sense pressure changes by responding to change in the tension of the arterial wall. The baroreflex mechanism is a fast response to changes in blood pressure.
Activation of SNS leads to;
1) Vasoconstriction of arterioles (Alpha-1 R mediated)
2) Reabsorption of tissue fluid
3) Increase venoconstriction of capillary vessels
4) Release of renin and RAAS activation
5) Increase in HR and Cardiac Contractility (B adrenergic effect)
ANG II
Acts on AT1-Receptors in VSMC to increase [Calcium] therefore creating vasoconstriction in arterioles.
Endocrine- Humoral Systems
Renin-Angiotensin-Aldosterone System (RAAS)
- When BP, Blood Vol., plasma Na+ fall, increased renal sympathetic drive that leads to B1-R mediated RENIN release.
- The outcome is increase BP
Renal B1-R Simulation
This will promote renin release, increasing vasoconstriction and BP
Renal B1-R Blockade
This will decrease renin production and decrease BP
Atenolol
B1-R Blocker at Kidney JG cells; decease BP
Aliskiren
Renin Inhibitor at the Kidney; decrease blood pressure
Enalapril
ACE Inhibitor at Lungs; decrease BP
Losartan
AT1-R blocker (ARB) at adrenal cortex; decrease BP
Spironolactone and Eplerenone
K+ SPARING diuretic in Kidney; decrease BP
ACE Inhibitors
Decrease ANG II which leads to;
- decreased sympathetic output
- increased vasodilation of vascular smooth muscle
- decrease retention of Na+ and H2O
- increased levels of Bradykinin
All leads to decreased BP
Vasopressin System; AVP
AKA ADH, plays major role in reabsorption of water from the collecting ducts of the kidneys
- restores plasma vol.
- increases AVP, BV, CO, BP
Atrial Natriuretic Peptide (ANP)
Is a powerful vasodilator, and a protein hormone secreted by heart muscle cells. It is involved in the homeostatic control of body water, sodium, potassium and fat (adipose tissue). It is released by muscle cells in the upper chambers (atria) of the heart (atrial myocytes) in response to high blood volume.
- Has both natriuretic and vasodilatory effects
Extrinsic Regulatory Systems
Primarily involved in regulation of BP and BV and include both nervous )SNS) and circulating hormonal systems (RAAS)
RAAS Recap
Major HUMORAL SYSTEM
- Ang II enhances sympathetic activation, vasoconstriction and aldosterone production to increase BP and BV
Endothelium Dependant Vasodilation
Effects adjacent vascular smooth muscle cell through release of Nitric Oxide (NO), Prostacyclin (PGI2) and EDHF from endothelial cells.
Nitric Oxide 1;
A powerful endothelial derived relaxing factor (vasodilator)
Nitric Oxide 2;
NO--> sGC--> increase cGMP--> decrease [Ca2+]--> Vasodilation
Prostacyclin
PGI2--> AC--> increase cAMP--> decrease [Ca+]--> Vasodilation
Drugs containing NO mechanisms
1) Hydrazine
2) Minoxidil
3) Sodium nitroprusside
All decrease TPR and BP, used as antihypertensives
Drugs that STIMULATE NO activity
1) Nitroglycerine
2) Isosorbide denitrate
Clinical management of angina
Endothelium Derived Hyperpolarizing Factor
EDHF--> K+ efflux--> Block Ca2+ channels; Ca2+ can't enter VSMC--> Vasodilation
Vascular Smooth Muscle Cell;
NO, PGI2 and EDHF released from EC decrease [Ca2+] in VSMC and promotes vasodilation and decreased BP.
Endothelin-1 (ET-1)
A peptide, is an endothelium derived contractile factor (vasoconstrictor)
Endothelin-1 Antagonists
Used to treat Pulmonary Hypertension. Ex, Ambrisentan (first choice) Bosentan (non-selective)
Secretion of Endothelin-1 from EC
ET-1 promotes Vasoconstriction in VSMC and increase BP via activation of Vascular Eta and Ebb receptors.
Ambrisentan
A selective Eta antagonist;
The peptide endothelin constricts muscles in blood vessels, increasing blood pressure. Ambrisentan, which relaxes those muscles, is an endothelin receptor antagonist, and is selective for the type A endothelin receptor
Bosentan
Bosentan is a dual endothelin receptor antagonist used in the treatment of pulmonary artery hypertension. Thus it is non-selective
Local (intrinsic) Control Systems
- Regulate blood flow within a tissue through myogenic stretch
- levels of pH, lactic acid, CO2
- Autacoids (Histamine, 5-HT, Eicosanoids [PG]
- any change in blood vessel tone
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