Pharmacology

• It is a sympathomimetic so it will do 1 of 2 things to allow more NE to hang out in the synapse
• 1. inhibit the reuptake of NE
• 2. increase the release of NE from the neuron

both of these result in stimulation of either the alpha-1 or beta-1 receptors

A beta-adrenergic agonist with an alpha antagonist

It refers to the ability of an alpha-1 agonist to reverse the vasoconstriction caused by high doses of Epi. This is why someone taking and alpha-1 will not have a pressor response to high doses of Epi.

• Prazosin
• As an alpha-1 antagonist it will cause vasodilation of vessels and there will be only a reflex increase in heart rate because the baroreceptors sense tone and the CNS will then activate an increase in parasympathetic firing resulting in vasodilation

Phentolamine is a non selective alpha antagonist so it will vasodilate vessels (alpha-1) BUT! it will also increase sympathetic firing (alpha-2) which will cause an even greater increase in heart rate

Demser will decrease the synthesis of both Epi & NE

S4 is the voltage sensing segment it is located on the alpha-1 subunit of the L type VGCC

Ionotropic effect will effect stroke volume


Chronotropic effect will effect heart rate

• alpha 1- Gq
• alpha 2- Gi
• beta 1- Gs
• beta 2- Gs

Proximal tubule

metabolic acidosis

Thin ascending loop & proximal tubule

Thick ascending limb

• hypokalemia
• hypocalcemia
• hypomagnesemia
• increased uric acid levels

distal convoluted tubule

• hypokalemia
• hypercalcemia

• late distal tubule
• collecting duct

hyperkalemia

• Late distal tubule
• Collecting duct

hyperkalemia

Compete with Cl ions to bind to the Na/K/2Cl transporter. When they bind and prevent the binding of Cl, the reabsorption of Na from the lumen is inhibited. Na is forced to enter the filtrate with water resulting in diuresis.

Osmotic diuretics are non-reabsorbable polysachharides that will increase extracellular osmolality. This causes diuresis because water will follow the osmotic diuretics to try to reduce osmolality and they are excreted in the process

Inhibit the Na/Cl symporter so the Na & Cl are being excreted into the filtrate instead of being reabsorbed

Blocks the binding of aldosterone to its receptors to prevent AIP (aldosterone induced protein) synthesis, so nothing will be able to activate the silent Na channels, so less Na is reabsorbed

Blocks carbonic anhydrase (CA) in the lumen and intracellularly. A lack of CA intracellularly means that there are no H ions in the proximal tubule, so Na can't be absorbed because there will be no Na/H exchange. We basically deplete the stores of H ion which will inhibit Na reabsorption.