Hello awesomites ! Some days back I revised my concepts on regulation of blood pressure so would like to share with you ,so lets start it .This is short -term regulation of blood pressure.
Changes in blood pressure is normally detected by 9th cranial nerve from carotid sinus and by 10th cranial nerve from aortic arch both of them carries signal to NTS (nucleus of tractus solitarius) present in medulla oblongata which in turn co-ordinate 3 centres present in medulla oblongata.
- Cardio inhibitory centre .
- Cardio stimulatory centre.
- Vasomotor centre.
Now suppose there is increase in blood pressure ,let's see microscopically what changes we are gonna seen in nerve endings of 9th and 10th nerve.
An increase in blood pressure will stretch carotid sinus and aortic arch ,which in turn will cause stretching or spreading of nerve endings ,which will increase influx of the sodium ions . Ultimately increase in depolarisation wave will cause stimulation of NTS (Even decrease in depolarisation wave will stimulate NTS ,which happens during decrease in blood pressure).Now as we know there is increase in blood pressure , NTS-our main character in this process will control these 3 centres to control blood pressure. Let's see what it do to these three centres present in medulla oblongata.
1)Cardio-inhibitory centre : This centre will be stimulated which in turn send fibers to SA node and AV node via right and left vagus nerve respectively.Leading to decrease in heart rate ,obviously cardiac output will decrease so will be blood pressure!.
2)Cardio-stimulatory centre: This centre will be inhibited which causes decrease in heart rate and cardiac output via it's fibers (post-ganglionic) which passes to lateral horn of spinal cord and then post-ganglionic fibers goes to sympathetic ganglion from where post-ganglionic sympathetic fibers acts on heart causing decrease in heart rate and cardiac output.
3)Vasomotor centre:This centre do's more work compared to above two mentioned centres .It acts on three areas ,
Arteries
Veins
Adrenal medulla
Let's see how it reacts when there is increase in blood pressure.
a) On arteries :It causes vasodilation leading to decrease in Total peripheral resistance which is directly proportional to diastolic pressure hence causes decrease in diastolic blood pressure.
b )On veins :It causes vasodilation leading to decrease in venous return which is directly proportional to EDV and which in turn causes decrease in Cardiac output and hence decrease in systolic blood pressure.
c )On adrenal medulla: Decreases release of epinephrine and nor-epinephrine which is responsible for decrease in HR,so decrease in blood pressure.
Woahh! Was such a long blog!
I think it's not necessary to mention occlusion of carotid artery causes false phenomenon of decrease in blood pressure so opposite effects will be seen:)
~Ojas.
Hi everyone,
this is notes on community medicine topic. levels of prevention and mode of intervention.
Hope it helps.
That's all
Shubham Patidar jmc 013
Hello awesomites ! Today I am gonna talk about a drug named as "Metoclopramide".
Basically it's a anti-emetic drug.First let us know what is emesis !.In simple words emesis means vomiting.Chemoreceptor trigger zone (CTZ) is located in area postrema and the nucleus tractus solitarius (NTS) of medulla oblongata.They both act as a important relay areas for afferent impulses arising in g.i.t.,throat and other viscera.
Metoclopramide is a Pro kinetic drug
It acts on GIT causing increase in peristaltic movement with relaxation of pylorus .
Mechanism of action includes :
a)D2 antagonism:It Decreases dopamine concentration and obviously acetylcholine concentration increases !.Which causes activation of ACh receptors leading to increase in LES tone and gastric pressure .
b)5-HT4 agonism:Activates 5-HT4 receptors on primary afferent neurons (PAN) of the ENS,via excitatory interneurons.
Gastric hurrying and LES tonic effects are mainly due to this action which is synergised by bethanechol and attenuated by atropine .
c)5-HT3 antagonism: At high concentrations it can block 5-HT3 receptors present on inhibitory myenteric interneurons and in NTS/CTZ .Increase in ACh concentration is also seen in minor condition
Long term use can cause parkinsonism-since decrease in dopamine , galactorrhea and gynecomastia .
It hastens use of many drugs like aspirin and diazepam by its action
~Jaskunwar Singh & Ojas
